Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 549
Page 549 20 Hypertension Hypertension is defined herein as sustained elevated arterial blood pressure measured indirectly by an inflatable cuff and pressure manometer. Hypertension can involve many organ systems, including the heart, endocrine organs, kidneys, and central and autonomic nervous systems. It has been clearly shown to increase the risk of developing stroke, coronary heart disease, congestive heart failure, peripheral vascular disease, and nephrosclerosis (Gordon and Kannel, 1972; Johansen, 1983; Stamler et al., 1980). Blood pressure is a continuously distributed variable in human populations, and the degree of cardiovascular risk is quantitatively related to the level of both systolic blood pressure (SBP) and diastolic blood pressure (DBP) throughout the entire range from highest to lowest (Kannel and Sorlie, 1975; Society of Actuaries, 1959). Thus, definitions of hypertension are arbitrary and serve only to classify people into risk categories and to analyze the effects of interventions designed to reduce blood pressure. An individual's blood pressure usually is not constant but varies to a certain extent from day to day. Many people with elevated blood pressure on one occasion will have lower levels at a second visit. Ordinarily, blood pressure must be measured on two or more separate visits before a diagnosis of hypertension is made. As a result, cross-sectional surveys in which blood pressure is measured on only one visit will usually result in an overestimate of the prevalence of sustained hypertension (JNC, 1984; Working Group on Risk and High Blood Pressure, 1985). The classification of blood pressure most commonly used is that of the World Health Organization (WHO) Expert Committee published in 1978 (WHO, 1978): · Normotension: SBP £ 140 mm Hg and DBP £ 90 mm Hg; · Borderline hypertension: SBP 141-159 mm Hg and DBP 91-94 mm Hg; ·Hypertension: SBP ³ 160 mm Hg or DBP ³ 95 mm Hg. Since borderline hypertension as well as isolated systolic hypertension (i.e., elevation of SBP without a concomitant increase in DBP) have been found to increase risk of cardiovascular diseases, a new classification has been promoted by the Third Joint National Committee (JNC III) for the Detection, Evaluation and Treatment of High Blood Pressure (JNC, 1984). JNC III classified adults with DBP between 85 and 89 mm Hg as "high normal" and reclassified some categories of patients into mild, moderate, and severe hypertension based on DBP criteria and into borderline and definite systolic hypertension based on SBP criteria. These definitions have been retained in the 1988 JNC report (JNC IV) and are given in Table 20-1 (JNC, 1988).
OCR for page 550
Page 550 TABLE 20-1 Classification of Blood Pressure in Adults 18 Years and Oldera Blood Pressure Range (mm Hg) Classificationb Diastolic <85 Normal blood pressure 85-89 High-normal blood pressure 90-104 Mild hypertension 105-114 Moderate hypertension ³ 115 Severe hypertension Systolic, when diastolic blood pressure is <90 <140 Normal blood pressure 140-159 Borderline isolated systolic hypertension ³ 160 Isolated systolic hypertension a Adapted from JNC (1988). Blood pressures are based on the average of two or more readings on two or more occasions. b A classification of borderline isolated systolic hypertension (SBP 140-159 mm Hg) or isolated systolic hypertension (SBP ³ 160 mm Hg) takes precedence over a classification of normal diastolic blood pressure (DBP < 85 mm Hg) or high-normal diastolic blood pressure (DBP 8589 mm Hg) when either occurs in the same person. A classification of high-normal diastolic blood pressure (DBP 85-89 mm Hg) takes precedence over a classification of normal systolic blood pressure (SBP < 140 mm Hg) when both occur in the same person. Population comparisons indicate that there are substantial differences in mean blood pressure values and distributions and in the frequency of adult hypertension that cannot be explained solely by problems of standardization and reliability of measurement. Data derived from the 1976-1980 National Health and Nutrition Examination Survey (NHANES II) conducted by the National Center for Health Statistics (Carroll et al., 1983) indicate that approximately 25 million adults in the United States (17.7%) have definite hypertension according to WHO criteria and that an additional 17 million (12.0%) have borderline hypertension (DHHS, 1986). If the JNC IV criteria are used, 42 million adults (29.7%) are hypertensive. Average SBP is higher among blacks than among whites in most adult age groups. Mean DBP is generally higher in men than in women and higher in black adults than in white adults. Isolated systolic hypertension was found to be rare below age 55 (DHHS, 1986). Comparison of NHANES II data (DHHS, 1986) with those from two previous surveysone during 1960-1962 (DHEW, 1963) and one during 1971-1975 (DHEW, 1979)indicates no significant trend in population mean or in distribution of average blood pressure for any ages between the 1960-1962 and 1971-1975 surveys, but NHANES II (1976-1980) showed a lower average SBP at all ages above 30 and a lower overall prevalence of hypertension in people over 40, based on either the WHO or the JNC IV criteria. The relative contributions to this possible lowering of average blood pressure made by detection and control programs and by primary prevention could not be determined from the data. Although both factors have probably played a role, there is no direct evidence of a decline in mean population blood pressure that is independent of medical treatment. Similarly, there is no evidence that the decline in high blood pressure has resulted from a change in the average weight of the population, since this has risen in recent years in the United States. Additional data on the distribution of hypertension in the population are given in Chapter 5. Evidence Associating Dietary Factors with Hypertension Human Studies The relationships among body mass, obesity, and hypertension have been extensively examined in human populations (see Chapter 21). In virtually every epidemiologic study of blood pressure throughout the world, investigators have found strong correlations between body mass and blood pressure and between obesity and hypertension. Although problems of measurement occur when cuff size is not properly adjusted to arm circumference in obese people, the relationship between body mass and blood pressure remains highly significant, even when this source of error is controlled. Blood pressure and body mass are well correlated in both the hypertensive and the normal ranges. Weight gain during adult life is associated with increased blood pressure levels. In the Framingham study, the risk of developing hypertension among those normotensive at entry was proportional to subsequent weight gain (Kannel et al., 1967). In general, risk appears greatest in people who gain weight during the third and fourth decades of life, after which the relationship weakens (Oberman et al., 1967; Stamler et al., 1975). Loss of weight by obese hypertensives is associated with a reduction in blood pressure, especially during active weight loss (Chiang et al., 1969; Reisin et al., 1978; Tuck et al., 1981; Tyroler et al., 1975). Little is known, however, about the effects of sustained weight loss
OCR for page 551
Page 551 on blood pressure. Moreover, the mechanisms by which body mass and obesity influence blood pressure are not well understood, and there are no established animal models for studying these relationships. The strongest body of evidence for an effect of nutrients on hypertension concerns the electrolytes sodium and potassium (see Chapter 15). No optimal range of salt intake has been established, and human populations vary widely in habitual intake. In many unacculturated societies where salt intake is habitually low (<4 g of salt per day), blood pressure does not rise with age, and hypertension is rare or absent (Page, 1979). There are no well-documented examples of societies that habitually ingest a moderately high-salt diet (approximately 6 g of salt or more per day) and in which hypertension is absent (Denton, 1984; Prineas and Blackburn, 1985). Many interpopulation comparisons show a positive correlation of salt intake with SBP as well as DBP (Froment et al., 1979; Gleibermann, 1973; Simpson, 1985), but the evidence is not entirely consistent (Intersalt Cooperative Research Group, 1988) (see Chapter 15). Studies of blood pressure and sodium intake or excretion within populations have also yielded inconsistent results, showing either a positive association (Kesteloot et al., 1980; Khaw and Barrett-Connor, 1988; Page et al., 1981; Tao et al., 1984) or no association (Dawber et al., 1967; Holden et al., 1983; Karvonen and Punsar, 1977; Ljungman et al., 1981; McCarron et al., 1982; Schlierf et al., 1980). The lack of association in many studies may reflect a high and relatively homogeneous salt intake within study populations; weaknesses in study design, including lack of control of potential confounding factors (e.g., obesity, sex, age, alcohol intake) (Prineas and Blackburn, 1985); or insufficient statistical power to detect a true association (Watt et al., 1983). Epidemiologic studies of populations with a high prevalence of hypertension (e.g., American blacks) have also demonstrated a positive correlation between salt intake and blood pressure level (Voors et al., 1983). In addition, studies of pressor responses to short-term changes in salt intake and salt depletion suggest that some people are more salt-responsive than others (Bittle et al., 1985; Fujita et al., 1980; Kawasaki et al., 1978; Luft et al., 1979a, 1982; Mark et al., 1975) and that responses are somewhat greater in hypertensives (Weinberger et al., 1986), in blacks of all ages, and in whites over the age of 40 (Luft et al., 1979b). Together, these data suggest that a habitual high-salt intake may increase the risk of developing hypertension. There is as yet, however, no certain method for identifying susceptible people or for ascertaining how many of them become hypertensive as a result of excessive salt intake. Dietary salt modification can be more effectively targeted when reliable genetic markers for identifying salt-sensitive people at increased risk for hypertension are identified. Low-potassium diets (e.g., 20 to 46 mEq/day) have been associated with increased risk of hypertension, stroke, and hypertension-related end-stage renal disease in several U.S. populations (Langford, 1985; Rostand et al., 1982; Walker et al., 1979) and elsewhere (Kromhout et al., 1985; Tobian, 1986). In addition, urinary sodium-to-potassium ratios have been positively correlated with DBP in several populations, even when no association with urinary sodium excretion was observed (Intersalt Cooperative Research Group, 1988; Langford, 1985; Page et al., 1981). Clinical studies show that supplemental potassium given to hypertensives can reduce SBP as much as 6 mm Hg and DBP as much as 4 mm Hg (Kaplan et al., 1985; MacGregor et al., 1982; Morino et al., 1978; Svetkey et al., 1986). Diets rich in natural sources of potassium have been associated with decreased rates of hypertension and stroke (Khaw and Barrett-Connor, 1984; Khaw and Rose, 1982; Kromhout et al., 1985; Reed et al., 1985). In a 12-year cohort study in people over age 50 in the United States, potassium intake was negatively correlated with stroke-related mortality. The inverse association remained even after controlling for age, caloric intake, SBP or DBP, dietary fiber, magnesium, and calcium (Khaw and Barrett-Connor, 1987). Within the past decade, a considerable amount of new evidence has been obtained about the role of dietary calcium in blood pressure regulation (see Chapter 13). However, no clear conclusions can be reached, partly because the differences in study results are not fully explained. In some epidemiologic studies, for example, reduced calcium intake was found to be the best dietary predictor of hypertension (Ackley et al., 1983; Garcia-Palmieri et al., 1984; Kok et al., 1986; McCarron et al., 1984), whereas other studies demonstrated no association (Feinleib et al., 1984; Gruchow et al., 1985) or even a positive association between level of calcium intake and blood pressure (Harlan et al., 1984). These varied findings may have resulted in part from the high degree of collinearity among other dietary components associated with blood pressure (e.g.,
OCR for page 552
Page 552 calcium, potassium, and protein) (Reed et al., 1985) and from limitations in the methods for assessing calcium intake in noninstitutionalized populations (Kaplan and Meese, 1986; Lau and Eby, 1985). Clinical findings have been more consistent than epidemiologic findings, demonstrating a mild, short-term reduction in blood pressure from calcium supplementation in some normotensives and hypertensives (Belizan et al., 1983; Grobbee and Hofman, 1986; McCarron and Morris, 1985; Resnick et al., 1984; Singer et al., 1985). However, in certain patients with hypertension and high levels of renin, blood pressure may increase (Resnick et al., 1984). As yet, there has been no clinical trial of calcium that is adequate in size and design. In population studies, consumption of more than two alcoholic drinks per day (>30 ml of alcohol per day) has generally been associated with a higher mean blood pressure and hypertension prevalence than found in those consuming lower levels of alcohol (Criqui, 1987) (see Chapter 16). Alcohol intake has also been associated with risk of hemorrhagic stroke and cerebral infarction in prospective studies (Donahue et al., 1986; Kagan et al., 1980, 1981) and case-control studies (Gill et al., 1986; Taylor et al., 1984; von Arbin et al., 1985). In the Framingham Offspring Study (Garrison et al., 1987), consumption of alcohol was associated with risk of hypertension after adjustment for adiposity and other variables in women but not in men. The reason for this difference is not clear, since the cross-sectional association between alcohol consumption and blood pressure level appears to be weaker in women than in men (Fortmann et al., 1983; Jackson et al., 1985; MacMahon and Leeder, 1984). In a randomized, crossover, single-blind study of alcohol restriction in mildly hypertensive Japanese office workers ages 30 to 59, Ueshima et al. (1987) found a modest reduction in SBP but not in DBP. Observational, clinical, and community intervention studies in humans suggest that a high ratio of dietary polyunsaturated to saturated fat (P/S) in the presence of low total fat produces a modest reduction in blood pressure in normotensive and mildly hypertensive people. The modest hypotensive effect of the high P/S diet was not evident in people consuming a low-salt (77 mM/day) diet (Puska et al., 1983). Studies on the relationship of protein intake to hypertension have yielded weak and inconsistent results (see Chapter 8). Chronically malnourished people exhibit low blood pressures (Viart, 1977), but the relative contribution of protein deficiency to this effect cannot be readily determined. Likewise, although epidemiologic studies have shown blood pressure levels (independent of age and weight) to be lower in populations consuming predominately vegetarian diets than in those consuming omnivorous diets (Armstrong et al., 1977; Ophir et al., 1983; Rouse and Beilin, 1984; Sacks et al., 1974), the findings cannot necessarily be ascribed to differences in plant and animal protein intakes, since it is likely that most types of vegetarians (complete vegetarians, lacto-ovovegetarians, and others) differ from omnivores in other dietary (e.g., lower fat and higher fiber intakes) and nondietary (e.g., lifestyle) factors that may confound the association between protein intake and blood pressure levels. Clinical findings are inconsistent, demonstrating either lower blood pressure levels in lacto-ovovegetarians than in omnivores (Rouse et al., 1983) or no difference in blood pressure (Brussaard et al., 1981). Epidemiologic studies of dietary fiber and blood pressure, like those of protein (see Chapter 10), indicate that blood pressures are lower in vegetarian populations than in omnivorous populations (Armstrong et al., 1977; Rouse et al., 1982; Sacks et al., 1974; Trowell, 1981). Clinical studies also indicate a fairly consistent blood pressure-lowering effect of high-fiber diets in normal as well as hypertensive subjects (Anderson, 1986; Dodson et al., 1984; Lindahl et al., 1984). Although study findings are fairly consistent, the potential influence of other dietary factors associated with these high-fiber diets (e.g., lower fat and animal protein; varied sodium, potassium, and calcium content) cannot be dismissed, nor can the findings be ascribed solely to an effect of dietary fiber. Other dietary factors have been studied in relation to hypertension. Lead, for example, has been associated with hypertension in several studies (Batuman et al., 1983; Beevers et al., 1980; Medeiros and Pellum, 1984), but there was no consistent relation to blood pressure in occupational studies and in studies of normotensives (see Chapter 14). This lack of consistency may in part reflect inadequate methods of measuring the body burden of lead (Batuman et al., 1983; Hansen and Pedersen, 1986). Pantothenic acid, magnesium, cadmium, chromium, and mercury have also been studied in relation to blood pressure levels, but again no consistent association in humans is apparent (see Chapters 12, 13, and 14).
OCR for page 553
Page 553 Animal Studies Experiments in animals provide strong evidence that salt intake plays a role in the causation of hypertension (see Chapter 15). The hypertensive effect of dietary salt is not observed in all animal models, but seems to operate most clearly when an underlying renal defect diminishes the ability to excrete salt rapidly (Tobian, 1983; Tobian et al., 1977). Studies indicate that Dahl S and Dahl R rats have blood pressures within the normal range when dietary salt is low, but the Dahl S rat has a slightly higher blood pressure than the Dahl R rat as well as some evidence of a defect in renal salt excretion. When both strains are fed a high-salt diet, the blood pressure of the Dahl R rat does not rise, whereas that of the Dahl S strain increases quickly and markedly (Dahl et al., 1962). The hypertensive effect of high-salt diets is also seen in other animal models with a diminished renal capacity to excrete salt, including the Kyoto spontaneously hypertensive rat (SHR) (Wilczynski and Leenen, 1987) and in animals given subtotal nephrectomy (Coleman and Guyton, 1969), injections of angiotensin (Muirhead et al., 1975), or doses of mineral corticoids sufficient to cause renal dysfunction and salt retention (Kaplan, 1982). These findings suggest that a combination of excessive dietary salt and reduced salt excretion may play a role in the development of hypertension in humans. This contention is consistent with epidemiologic evidence that populations with a lifelong low-salt diet seem to have no hypertension whatsoever and evidence from human genetics that susceptibility to hypertension may be related to a diminished capacity for rapid sodium excretion (Grim et al., 1979). Supplemental potassium moderates the effects of hypertension in susceptible animals. Although the addition of potassium reduces blood pressure only modestly (Tobian et al., 1985), it appears to retard the gradual progressive changes in renal structure and function seen in hypertensive animals, including progressive destruction of the kidney tubules. High-potassium diets also prevent injury to the endothelial cells in many arteries. This may explain why such diets prevent much of the thickening of the intimal and medial layers of arteries in susceptible animals and preserve endothelium-dependent relaxation in their arteries (Tobian et al., 1984, 1987). The addition of potassium to high-salt diets also markedly decreases stroke incidence and overall mortality in stroke-prone spontaneously hypertensive rats and Dahl S rats (Tobian et al., 1985) as well as in Sprague-Dawley rats (Meneely and Ball, 1958). It also protects against the vascular lesions observed in arteries of hypertensive rabbits (Gordon and Drury, 1956) and rats (Goldby and Beilin, 1972; Tobian, 1986), which could explain the reduction in stroke mortality. The mechanism by which increased dietary potassium protects against endothelial and vascular injury is not known. In most animal models (see Chapter 15), nonchloride salts failed to elevate blood pressure (Berghof and Geraci, 1929; Kurtz and Morris, 1985; Whitescarver et al., 1984). These data suggest that both sodium and chloride are necessary to produce hypertension in these animal models, but more studies on the effects of different salts are needed. A number of animal studies indicate that calcium supplementation can lower blood pressure in the spontaneously hypertensive rat (Ayachi, 1979; Kageyama et al., 1986; Lau et al., 1984; McCarron et al., 1981, 1985), but that the effect is not produced consistently in normotensive control animals, such as the Wistar-Kyoto rat (see Chapter 13). There is insufficient experimental evidence to support an inverse association between dietary calcium and blood pressure level. Studies of dietary fatty acids and blood pressure in animals suggest that diets deficient in linoleic acid increase blood pressure (see Chapter 7) and that the addition of linoleic acid to a low-fat, low-salt diet can decrease blood pressure (Düsing et al., 1983; MacDonald et al., 1981; Moritz et al., 1985). Cadmium exposure has been linked to increased hypertension risk in animal studies, but the findings are inconsistent and possible mechanisms of action are not known (see Chapter 14). Cadmium doses insufficient to produce other signs of cadmium toxicity have induced hypertension in some studies, but in others, doses high enough to produce chronic toxicity had no effect (Eakin et al., 1980; Fingerle et al., 1982; Whanger, 1979). Perry and Kopp (1983) suggested that the presence of other trace elements such as selenium, copper, and zinc may counteract the hypertensive action of cadmium, but this has not been confirmed. Other dietary factors, including protein, pantothenic acid, chromium, mercury, lead, and fluoride, have also been examined in relation to hypertension (see Chapters 8, 12, and 14). None of the laboratory studies has provided convincing evidence of a relationship between these factors and blood pressure levels.
OCR for page 554
Page 554 Evidence Associating Nondietary Factors with Hypertension Heredity A genetic predisposition to hypertension is generally acknowledged both for humans and laboratory animals (Folkow, 1982). Although it has not been determined whether a single gene (McManus, 1983; Platt, 1947) or polygenic inheritance (Folkow, 1982) is involved, the current consensus is that for humans, the predisposition is polygenic and permissive rather than determinative. Thus, the tendency to develop hypertension remains latent unless one or more environmental influences activate the mechanisms that raise blood pressure. Primary hypertension in humans probably does not result from genetic influences alone. Because predisposition of humans to hypertension is polygenic, it is probable that different genes or gene products are activated or suppressed by single or multiple environmental influences, including sodium and potassium intake, psychosocial stress, and other environmental or nutritional influences. The resulting effect on blood pressure may in turn affect cardiovascular control mechanisms involving endocrine, renal, or cardiac factors, the central nervous system, or other systems. Thus, the factors triggering the onset, progression, and outcome of hypertension in genetically susceptible individuals are probably many and varied (Folkow, 1982). Because of the complexity of genetic composition, it is unlikely that a single uniform cause of hypertension in humans will be found. It is nevertheless possible that some predisposing constellations of genetic factors may occur commonly in humans. Furthermore, one or more environmental factors may initiate a cascade of physiological events that lead to hypertension, even after the initiating factors are no longer operating. There is considerable variety in the factors triggering hypertension among the various strains of genetically susceptible rodents. As described above, the Dahl S and R rat strains differ strikingly in their response to salt loading (Dahl et al., 1962). The SHR strain (Okamoto and Aoki, 1963) is sensitive to sodium loading as well as psychosocial stimuli, but will develop hypertension without either. The Milan hypertensive rat is also sensitive to salt loading but not to psychological stimuli (Folkow, 1982; Hallback et al., 1977). The variety of precipitating factors is more complex in humans because of our greater genetic heterogeneity, far more complex environment, and longer lifespan. Strong evidence exists for interaction of genetic predisposition with electrolytes and obesity. Evidence for the role of other nutrients, psychosocial stress, and other influences is weaker and less consistent. Studies in humans have provided strong evidence of similar blood pressures among twins, siblings, and other first-degree relatives (Feinleib et al., 1975; Miller and Grim, 1983; Zinner et al., 1971). However, efforts to identify genetic markers for susceptibility to hypertension or for sodium sensitivity have not been successful (see Chapter 15). Apart from relatively crude and qualitative indicators derived from knowledge of blood pressure in relatives, no valid method exists for predicting susceptibility to hypertension. Racial Influences Many studies demonstrate that blood pressure is higher and hypertension more prevalent among blacks of African origin than in Caucasians living in similar environments (Stamler et al., 1975). This has been borne out in three surveys of blood pressure by the National Center for Health Statistics (DHHS, 1986). It is possible that a variety of genetic, physiological, dietary, and psychosocial influences are important in producing these differences. Comparisons of black and white schoolchildren show differences in plasma renin activity, dopamine b-hydroxylase activity, glucose tolerance, and resting heart rate (Berenson, 1980). Several studies demonstrate marked differences between black and white Americans in dietary intake and excretion of sodium and potassium (Cushman and Langford, 1983; Grim et al., 1980) and in response to acute sodium loading (Luft et al., 1979b). Among black and white hypertensives, there may also be differences in sodium-lithium countertransport in blood cells (Canessa et al., 1984) and in response to different classes of antihypertensive medications (Cushman and Langford, 1983). Differences in blood pressure among other racial groups have also been reported (DHHS, 1985), but data are not sufficiently extensive or of high enough quality to permit firm conclusions to be drawn. Psychosocial and Sociocultural Influences Although many studies have related short-term changes in blood pressure to psychosocial and
OCR for page 555
Page 555 sociocultural factors, little is known about how these factors might interact with diet to increase risk of sustained hypertension. This is undoubtedly due in part to the heterogeneity of subjects, the complexity of blood pressure control mechanisms, and the complexity of the psychosocial environment. Cross-sectional and longitudinal studies of populations undergoing a cultural change from traditional to more westernized or industrialized ways of life usually show an increase in both SBP and DBP (Cassel, 1975; Cruz-Coke et al., 1973; Maddocks, 1967; Page et al., 1974; Sever et al., 1980). Such increases have been observed in migrants and in populations undergoing rapid industrialization (Beaglehole et al., 1977; Page and Friedlaender, 1986; Poulter et al., 1985; Prior et al., 1977). When other factors, such as change in body weight or diet are controlled, however, variance in blood pressure due to such environmental factors as psychosocial stress appears to be small. For example, in a longitudinal study of Polynesians who migrated from the Tokelau Islands to New Zealand, Beaglehole et al. (1977) found that the degree of social interactions with white New Zealanders accounted for only 2.1% of the blood pressure variance in males and 1.4% in females after controlling for dietary change. In a study of migrants who relocated from a rural tribal area in Kenya to Nairobi, Poulter et al. (1985) found that SBP and DBP were elevated within the first 60 days after migration and that intake of sodium, potassium, calcium, and other nutrients had also changed. Exercise and Activity Many studies have focused on the effects of activity and exercise in both hypertensive and normotensive people (Berkson et al., 1960; Bonanno and Lies, 1974; De Vries, 1970; Jennings et al., 1984; Urata et al., 1987), but the long-term hypotensive effects of activity and exercise have not been studied. Furthermore, most studies on this topic are poorly designed, lack appropriate control subjects (Leon and Blackburn, 1982), and have not demonstrated an association with dietary factors. Pediatric Diet and Adult Hypertension The relationship of blood pressure in childhood to adult hypertension has not been clearly established. The inconsistency in study findings may relate in part to the difficulty of obtaining accurate blood pressure readings in children (Berenson, 1980; Lauer and Clarke, 1980). Two studies of cardiovascular risk factors in schoolchildren (Berenson et al., 1980; Lauer and Clarke, 1980) demonstrate a strong relationship between body size and blood pressure during growth but do not show a strong relationship of blood pressure to diet or to specific nutrients. Children tend to remain in the same percentile of SBP and DBP relative to their peers until adolescence (Lauer and Clarke, 1980). Differences between blacks and whites are small during infancy and early childhood (Berenson et al., 1980; Schacter et al., 1982) but become stronger during adolescence (Berenson et al., 1980). Few intervention studies have been conducted in infants and children. In one randomized trial of sodium intake and blood pressure during the first 6 months of life, infants who consumed a low-salt formula approximating the salt content of human breast milk (365 mg of sodium chloride per liter) had an SBP slightly lower than in those on normal formula (1,100 mg of sodium chloride per liter) (Hofman et al., 1983). Growth rate and body size were the same in the two groups. After 1 year, there were no differences in blood pressure between the two groups. In a study conducted in China by Kangmim et al. (1987), no single nutrient was correlated with blood pressure in boys ages 7 and 8, although the ratios of sodium to potassium and potassium to calcium were correlated with SBP in multivariate analyses. Summary Frequency of high blood pressure, average blood pressure, and population distributions of blood pressures vary widely among populations. Some populations are characterized by a rarity of adult hypertension and the absence of an increase in blood pressure with age. Others, such as the U.S. population, are characterized by an increase in blood pressure with age and a high prevalence of hypertension among adults. In such populations, where exposure to environmental factors affecting blood pressure is presumably widespread, familial and genetic factors appear to have a strong influence on individual blood pressure levels. Obesity and habitual high-alcohol intake appear to be associated with an increased risk of hypertension. Habitual high-salt intake appears to have a major adverse effect on hypertension risk in some
OCR for page 556
Page 556 susceptible people, but there is no certain method for identifying such people or ascertaining how many of them will become hypertensive as a result of excessive salt intake. Potassium may modulate the blood pressure-raising effects of sodium and provide some protection against death from stroke, even when blood pressure is not reduced. Some evidence suggests that reduced fat intake and a high P/S ratio also reduce blood pressure. Data on calcium are inconclusive. Psychosocial and sociocultural factors affecting risk of sustained hypertension are also inconclusive, and no linkage to diet has been reported. Some data suggest that increased physical activity and exercise have a long-term hypotensive effect, either independently or in association with diet. Directions for Research · The mechanisms by which nutrients affect the development of hypertension. Such research should further examine the effects and interactions of sodium, potassium, calcium, alcohol, lipids, and proteins of different origin and composition. · The combined action of diet and physical fitness on blood pressure. · Nutrient consumption, with particular attention to foods and nutrients known to influence blood pressure. · Racial differences in blood pressure level and risk of hypertension, particularly in respect to the higher risks of hypertension and hypertension-related mortality in blacks compared to whites. · The pediatric antecedents, dietary and other, of adult hypertension through the continued application of longitudinal study. · Identification of genetic markers of susceptability to dietary effects on blood pressure. References Ackley, S., E. Barrett-Connor, and L. Suarez. 1983. Dairy products, calcium and blood pressure. Am. J. Clin. Nutr. 38:457-461. Anderson, J.W. 1986. High-fiber, hypocaloric vs very-low-calorie diet effects on blood pressure of obese men. Am. J. Clin. Nutr. 43:695. Armstrong, B., H. Coates, and A.J. van Merwyk. 1977. Blood pressure in Seventh-Day Adventist vegetarians. Am. J. Epidemiol. 105:444-449. Ayachi, S. 1979. Increased dietary calcium lowers blood pressure in the spontaneously hypertensive rat. Metabolism 28:1234-1238. Batuman, V., E. Landy, J.K. Maesaka, and R.P. Wedeen. 1983. Contribution of lead to hypertension with renal impairment. N. Engl. J. Med. 309:17-21. Beaglehole, R., C.E. Salmond, A. Hooper, J. Huntsman, J.M. Stanhope, J.C. Cassel, and I.A. Prior. 1977. Blood pressure and social interaction in Tokelauan migrants in New Zealand. J. Chronic Dis. 30:803-812. Beevers, D.G., J.K. Cruickshank, W.B. Yeoman, G.F. Carter, A. Goldberg, and M.R. Moore. 1980. Blood-lead and cadmium in human hypertension. J. Environ. Pathol. Toxicol. 4:251-260. Belizan, J.M., J. Villar, O. Pineda, A.E. Gonzalez, E. Sainz, G. Garrera, and R. Sibrian. 1983. Reduction of blood pressure with calcium supplementation in young adults. J. Am. Med. Assoc. 249:1161-1165. Berenson, G.S. 1980. Cardiovascular Risk Factors in Children. Oxford University Press, New York. 453 pp. Berenson, G.S., A.W. Voors, and L.S. Webber. 1980. Importance of blood pressures in children. Pp. 71-97 in H. Kesteloot and J.V. Joossens, eds. Epidemiology of Arterial Blood Pressure: Developments in Cardiovascular Medicine, Vol. 8. Martinus Nijhoff, The Hague. Berghoff, R.S., and A.S. Geraci. 1929. Influence of sodium chloride on blood pressure. III. Med. J. 56:395-397. Berkson, D.M., J. Stamler, H.A. Lindberg, W. Miller, H. Mathies, H. Lasky, and Y. Hall. 1960. Socioeconomic correlates of atherosclerotic and hypertensive heart diseases. Ann. N.Y. Acad. Sci. 84:835-850. Bittle, C.C., Jr., D.J. Molina, and F.C. Bartter. 1985. Salt sensitivity in essential hypertension as determined by the Cosinor method. Hypertension 7:989-994. Bonanno, J.A., and J.E. Lies. 1974. Effects of physical training on coronary risk factors. Am. J. Cardiol. 33:760-764. Brussaard, J.H., J.M. van Raaij, M. Stasse-Wolthuis, M.B. Katan, and J.G. Hautvast. 1981. Blood pressure and diet in normotensive volunteers: absence of an effect of dietary fiber, protein, or fat. Am. J. Clin. Nutr. 34:2023-2029. Canessa, M., A. Spalvins, N. Adragna, and B. Falkner. 1984. Red cell sodium countertransport and cotransport in normotensive and hypertensive blacks. Hypertension 6:344-351. Carroll, M.D., S. Abraham, and C.M. Dresser. 1983. Dietary Intake Source Data: United States, 1976-80. Vital and Health Statistics, Ser. 11, No. 231. DHHS Publ. No. (PHS) 83-1681. National Center for Health Statistics, Public Health Service, U.S. Department of Health and Human Services, Hyattsville, Md. 483 pp. Cassel, J. 1975. Studies of hypertension in migrants. Pp. 41-58 in O. Paul, ed. Epidemiology and Control of Hypertension. Stratton Intercontinental Medical Book Co., New York. Chiang, B.N., L.V. Perlman, and F.H. Epstein. 1969. Overweight and hypertension: a review. Circulation 39:403-421. Coleman, T.G., and A.C. Guyton. 1969. Hypertension caused by salt loading in the dog. III. Onset transients of cardiac output and other circulatory variables. Circ. Res. 25: 153-160. Criqui, M.H. 1987. Alcohol and hypertension: new insights from population studies. Euro. Heart J. 8 Suppl. B:19-26. Cruz-Coke, R., H. Donoso, and R. Berrera. 1973. Genetic ecology of hypertension. Clin. Sci. Mol. Med. 45:55s-65s. Cushman, W.C., and H.G. Langford. 1983. Urinary electrolyte differences in black and white hypertensives: Veterans Administration Cooperative Study Group on antihypertensive agents. Clin. Res. 31:843A. Dahl, L.K., M. Heine, and L. Tassinari. 1962. Effects of chronic excess salt ingestion. Evidence that genetic factors
OCR for page 557
Page 557 play an important role in susceptibility to experimental hypertension. J. Exp. Med. 115:1173-1190. Dawber, T.R., W.B. Kannel, A. Kagan, R.K. Donabedian, P.M. McNamara, and G. Pearson. 1967. Environmental factors in hypertension. Pp. 255-288 in J. Stamler, R. Stamler, and T.N. Pullman, eds. The Epidemiology of Hypertension. Grune and Stratton, New York. Denton, D. 1984. The Hunger for Salt: An Anthropological, Physiological and Medical Analysis. Springer-Verlag, Berlin. 650 pp. De Vries, H.A. 1970. Physiological effects of an exercise training regimen upon men aged 52 to 88. J. Gerontol. 25:325-336. DHEW (U.S. Department of Health, Education, and Welfare). 1963. Origin, Program, and Operation of the U.S. National Health Survey. Vital and Health Statistics, Ser. 1, No. 1. PHS Publ. No. 1000. National Center for Health Statistics, Public Health Service, U.S. Department of Health, Education, and Welfare, Washington, D.C. 41 pp. DHEW (U.S. Department of Health, Education, and Welfare). 1979. Dietary Intake Source Data: United States, 1971-74. DHEW Publ. No. (PHS) 79-1221. National Center for Health Statistics, Public Health Service, U.S. Department of Health, Education, and Welfare, Hyattsville, Md. 421 pp. DHHS (U.S. Department of Health and Human Services). 1985. Plan and Operation of the Hispanic Health and Nutrition Examination Survey 1982-84. Vital and Health Statistics, Ser. 1, No. 19. DHHS Publ. No. (PHS) 85-1321. National Center for Health Statistics, Public Health Service, U.S. Department of Health and Human Services, Hyattsville, Md. 429 pp. DHHS (U.S. Department of Health and Human Services). 1986. Blood Pressure Levels in Persons 18-74 Years of Age in 1976-80, and Trends in Blood Pressure from 1960 to 1980 in the United States. Data from the National Health Survey, Ser. 11, No. 234. DHHS Publ. No. (PHS) 86-1684. National Center for Health Statistics, Public Health Service, U.S. Department of Health and Human Services, Hyattsville, Md. 68 pp. Dodson, P.M., P.J. Pacy, P. Bal, A.J. Kubicki, R.F. Fletcher, and K.G. Taylor. 1984. A controlled trial of a high fibre, low fat and low sodium diet for mild hypertension in Type 2 (non-insulin-dependent) diabetic patients. Diabetologia 27: 522-526. Donahue, R.P., R.D. Abbott, D.M. Reed, and K. Yano. 1986. Alcohol and hemorrhagic stroke. J. Am. Med. Assoc. 255:2311-2314. Düsing, R., R. Scherhag, K. Glänzer, U. Budde, and H.J. Kramer. 1983. Dietary linoleic acid deprivation: effects on blood pressure and PGI2 synthesis. Am. J. Physiol. 244: H228-H233. Eakin, D.J., L.A. Schroeder, P.D. Whanger, and P.H. Weswig. 1980. Cadmium and nickel influence on blood pressure, plasma renin, and tissue mineral concentrations. Am. J. Physiol. 238:E53-E61. Feinleib, M., C. Lenfant, and S.A. Miller. 1984. Hypertension and calcium. Science 226:384-389. Feinleib, M., R. Garrison, N. Borhani, R. Rosenman, and J. Christian. 1975. Studies of hypertension in twins. Pp. 3-20 in O. Paul, ed. Epidemiology and Control of Hypertension. Stratton Intercontinental Medical Book Co., New York. Fingerle, H., G. Fischer, and H.G. Classen. 1982. Failure to produce hypertension in rats by chronic exposure to cadmium. Food Chem. Toxicol. 20:301-306. Folkow, B. 1982. Physiological aspects of primary hypertension. Physiol. Rev. 62:347-504. Fortmann, S.P., W.L. Haskell, K. Vranizan, B.W. Brown, and J.W. Farquhar. 1983. The association of blood pressure and dietary alcohol: differences by age, sex, and estrogen use. Am. J. Epidemiol. 118:497-507. Froment, A., H. Milon, and C. Gravier. 1979. Relationship of sodium intake and arterial hypertension: contribution of geographical epidemiology. Rev. Epidemiol. Sante Publique 27:437-454. Fujita, T., W.L. Henry, F.C. Bartter, C.R. Lake, and LS. Delea. 1980. Factors influencing blood pressure in salt-sensitive patients with hypertension. Am. J. Med. 69:334-344. Garcia-Palmieri, M.R., R. Costas, Jr., M. Cruz-Vidal, P.D. Sorlie, J. Tillotson, and R.J. Havlik. 1984. Milk consumption, calcium intake, and decreased hypertension in Puerto Rico. Puerto Rico Heart Health Program study. Hypertension 6:322-328. Garrison, R.J., W.B. Kannel, J. Stokes III, and W.P. Castelli. 1987. Incidence and precursors of hypertension in young adults: the Framingham Offspring Study. Prev. Med. 16: 235-251. Gill, J.S., A.V. Zezulka, M.J. Shipley, S.K. Gill, and G. Beevers. 1986. Stroke and alcohol consumption. N. Engl. J. Med. 315:1041-1046. Gleibermann, L. 1973. Blood pressure and dietary salt in human populations. Ecol. Food Nutr. 2:143-156. Goldby, F.S., and L.J. Beilin. 1972. Relationship between arterial pressure and the permeability of arterioles to carbon particles in acute hypertension in the rat. Cardiovasc. Res. 6:384-390. Gordon, D.B., and D.R. Drury. 1956. Effect of potassium on occurrence of petechial hemorrhages in renal hypertensive rabbits. Circ. Res. 4:167-172. Gordon, T., and W.B. Kannel. 1972. Predisposition to atherosclerosis in the head, heart, and legs. J. Am. Med. Assoc. 221:661-666. Grim, C.E., F.C. Luft, J.Z. Miller, P.L. Brown, M.A. Gannon, and M.H. Weinberger. 1979. Sodium labeling and depletion in normotensive first degree relatives of essential hypertensives. J. Lab. Clin. Med. 94:764-771. Grim, C.E, F.C. Luft, J.Z. Miller, G.R. Meneely, H.D. Battarbee, C.G. Hames, and L.K. Dahl. 1980. Racial difference in blood pressure in Evans County, Georgia: relationship to sodium and potassium intake and plasma renin activity. J. Chronic Dis. 33:87-94. Grobbee, D.E., and A. Hofman. 1986. Effect of calcium supplementation on diastolic blood pressure in young people with mild hypertension. Lancet 2:703-707. Gruchow, H.W., K.A. Sobocinski, and .J. Barboriak. 1985. Alcohol, nutrient intake, and hypertension in U.S. adults. J. Am. Med. Assoc. 253:1567-1570. Hallback, M., J.V. Jones, G. Bianchi, and B. Folkow. 1977. Cardiovascular control in the Milan strain of spontaneously hypertensive rat (MHS) at ''rest" and during acute mental "stress." Acta Physiol. Scand. 99:208-216. Hansen, J.C., and H.S. Pedersen. 1986. Environmental exposure to heavy metals in North Greenland. Arct. Med. Res. 41:21-34. Harlan, W.R., A.L. Hull, R.L. Schmouder, J.R. Landis, F.E. Thompson, and F.A. Larkin. 1984. Blood pressure and nutrition in adults. The National Health and Nutrition Examination Survey. Am. J. Epidemiol. 120:17-18.
OCR for page 558
Page 558 Hofman, A., A. Hazebroek, and H.A. Valkenburg. 1983. A randomized trial of sodium intake and blood pressure in newborn infants. J. Am. Med. Assoc. 250:370-373. Holden, R.A., A.M. Ostfeld, D.H. Freeman, Jr., K.G. Hellenbrand, and D.A. D'Atri. 1983. Dietary salt intake and blood pressure. J. Am. Med. Assoc. 250:365-369. Intersalt Cooperative Research Group. 1988. Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Br. Med. J. 297:319-328. Jackson, R., A. Stewart, R. Beaglehole, and R. Scragg. 1985. Alcohol consumption and blood pressure. Am. J. Epidemiol. 122:1037-1044. Jennings, G.L., L. Nelson, M.D. Esler, P. Leonard, and P.I. Korner. 1984. Effects of changes in physical activity on blood pressure and sympathetic tone. J. Hypertens. 2 Suppl. 3:139-141. Johansen, H.L. 1983. Hypertension in Canada: risk factor review and recommendations for further work. Can. J. Public Health 74:123-128. JNC (Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure). 1984. The 1984 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch. Intern. Med. 144:1045-1057. JNC (Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure). 1988. The 1988 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch. intern. Med. 148:1023-1038. Kagan, A., J.S. Popper, and G.G. Rhoads. 1980. Factors related to stroke incidence in Hawaii Japanese men. The Honolulu Heart Study. Stroke 11:14-21. Kagan, A., K. Yano, G.G. Rhoads, and D.L. McGee. 1981. Alcohol and cardiovascular disease: the Hawaiian experience. Circulation 64:27-31. Kageyama, Y., H. Suzuki, K. Hayashi, and T. Saruta. 1986. Effects of calcium loading on blood pressure in spontaneously hypertensive rats: attenuation of the vascular reactivity. Clin. Exp. Hypertens. 8:355-370. Kangmim, Z., H. Shangpu, P. Xiaoqin, Z. Xianrong, and G. Yuan. 1987. The relation of urinary cations to blood pressure in boys aged seven to eight years. Am. J. Epidemiol. 126:658-663. Kannel, W.B., and P. Sorlie. 1975. Hypertension in Framingham. Pp. 553-592 in O. Paul, ed. Epidemiology and Control of Hypertension. Stratton Intercontinental Medical Book Co., New York. Kannel, W.B., N. Brand, J.J. Skinner, Jr., T.R. Dawber, and P. McNamara. 1967. The relation of adiposity to blood pressure and the development of hypertension. The Framingham Study. Ann. Intern. Med. 67:48-59. Kaplan, N.M.. 1982. Clinical Hypertension, 3rd ed. Williams and Wilkins, Baltimore. 454 pp. Kaplan, N.M., and R.B. Meese. 1986. The calcium deficiency hypothesis of hypertension: a critique. Ann. intern. Med. 105:947-955. Kaplan, N.M., A. Carnegie, P. Raskin, J.A. Heller, and M. Simmons. 1985. Potassium supplementation in hypertensive patients with diuretic-induced hypokalemia. N. Engl. J. Med. 312:746-749. Karvonen, M.J., and S. Punsar. 1977. Sodium excretion and blood pressure of West and East Finns. Acta Med. Scand. 202:501-507. Kawasaki, T., C.S. Delea, F.C. Bartter, and H. Smith. 1978. The effect of high-sodium and low-sodium intakes on blood pressure and other related variables in human subjects with idiopathic hypertension. Am. J. Med. 64:193-198. Kesteloot, H., B.C. Park, C.S. Lee, E. Brems-Heyns, J. Claessens, and J.V. Joossens. 1980. A comparative study of blood pressure and sodium intake in Belgium and in Korea. Eur. J. Cardiol. 11:169-182. Khaw, K.T., and E. Barrett-Connor. 1984. Dietary potassium and blood pressure in a population. Am. J. Clin. Nutr. 39: 963-968. Khaw, K.T., and E. Barrett-Connor. 1987. Dietary potassium and stroke-associated mortality: a 12-year prospective population study. N. Engl. J. Med. 316:235-240. Khaw, K.T., and E. Barrett-Connor. 1988. The association between blood pressure, age, and dietary sodium and potassium: a population study. Circulation 77:53-61. Khaw, K.T., and G. Rose. 1982. Population study of blood pressure and associated factors in St. Lucia, West Indies. Int. J. Epidemiol. 11:372-377. Kok, F.J., J.P. Vandenbroucke, C. van der Heide-Wessel, and R.M. van-der Heide. 1986. Dietary sodium, calcium, and potassium, and blood pressure. Am. J. Epidemiol. 123: 1043-1048. Kromhout, D., E.B. Bosschieter, and C.D. Coulander. 1985. Potassium, calcium, alcohol intake and blood pressure: the Zutphen Study. Am. J. Clin. Nutr. 41:1299-1304. Kurtz, T.W., and R.C. Morris, Jr. 1985. Dietary chloride as a determinant of disordered calcium metabolism in salt-dependent hypertension. Life Sci. 36:921-929. Langford, H.G. 1985. Potassium and hypertension. Pp. 147-153 in M.J. Horan, M. Blaustein, J.B. Dunbar, W. Kachadorian, N.M. Kaplan, and A.P. Simopoulos, eds. NIH Workshop on Nutrition and Hypertension: Proceedings from a Symposium. Biomedical Information Corp., New York. Lau, K., and B. Eby. 1985. The role of calcium in genetic hypertension. Hypertension 7:657-667. Lau, K., D. Zikos, J. Spirnak, and B. Eby. 1984. Evidence for an intestinal mechanism in hypercalciuria of spontaneously hypertensive rats. Am. J. Physiol. 247:E625-E633. Lauer, R.M., and W.R Clarke. 1980. Immediate and long-term prognostic significance of childhood blood pressure levels. Pp. 281-290 in R.M. Lauer and RB. Shekelle, eds. Childhood Prevention of Atherosclerosis and Hypertension. Raven Press, New York. Leon, A.S. and H. Blackburn. 1982. Physical activity and hypertension. Pp. 14-36 in P. Sleight and E. Freis, eds. Hypertension: Cardiology, Vol. 1. Butterworth Scientific, London. Lindahl, O., L. Lindwall, A. Spangberg, A. Stenram, and P.A. Ockerman. 1984. A vegan regimen with reduced medication in the treatment of hypertension. Br. J. Nutr. 52:11-20. Ljungman, S., M. Aurell, M. Hartford, J. Wikstrand, L Wilhelmsen, and G. Berglund. 1981. Sodium excretion and blood pressure. Hypertension 3:318-326. Luft, F.C., LI. Rankin, R. Bloch, A.E. Weyman, L.R. Willis, R.H. Murray, C.E. Grim, and M.H. Weinberger. 1979a. Cardiovascular and humoral responses to extremes of sodium intake in normal black and white men. Circulation 60:697-706. Luft, F.C., C.E Grim, N. Fineberg, and M.C. Weinberger. 1979b. Effects of volume expansion and contraction in
OCR for page 559
Page 559 normotensive whites, blacks, and subjects of different ages. Circulation 59:643-650. Luft, F.C., M.H. Weinberger, and C.E. Grim. 1982. Sodium sensitivity and resistance in normotensive humans. Am. J. Med. 72:726-736. MacDonald, M.C., R.L. Kline, and G.J. Mogenson. 1981. Dietary linoleic acid and salt-induced hypertension. Can. J. Physiol. Pharmacol. 59:872-875. MacGregor, G.A., S.J. Smith, N.D. Markandu, R.A. Banks, and G.A. Sagnella. 1982. Moderate potassium supplementation in essential hypertension. Lancet 2:567-570. MacMahon, S.W., and S.R. Leeder. 1984. Blood pressure levels and mortality from cerebrovascular disease in Australia and the United States. Am. J. Epidemiol. 120:865-875. Maddocks, I. 1967. Blood pressure in Melanesians. Med. J. Aust. 1:1123-1126. Mark, A.L, W.J. Lawton, F.M. Abboud, A.E. Fitz, W.E. Connor, and D.D. Heistad. 1975. Effects of high and low sodium intake on arterial pressure and forearm vascular resistance in borderline hypertension. A preliminary report. Circ. Res. 36 Suppl. 1:194-198. McCarron, D.A., and C.D. Morris. 1985. Blood pressure response to oral calcium in persons with mild to moderate hypertension. A randomized, double-blind, placebo-controlled, crossover trial. Ann. Intern. Med. 103:825-831. McCarron, D.A., N.N. Yung, B.A. Ugoretz, and S. Krutzik. 1981. Disturbances of calcium metabolism in the spontaneously hypertensive rat. Hypertension 3:I162-I167. McCarron, D.A., H.J. Henry, and C.D. Morris. 1982. Human nutrition and blood pressure regulation: an integrated approach. Hypertension 4:III2-III13. McCarron, D.A., C.D. Morris, H.J. Henry, and J.L Stanton. 1984. Blood pressure and nutrient intake in the United States. Science 224:1392-1398. McCarron, D.A., P.A. Lucas, R.J. Shneidman, B. LaCour, and R. Drëke. 1985. Blood pressure development of the spontaneously hypertensive rat after concurrent manipulations of dietary Ca2+ and Na+. Relation to intestinal fluxes. J. Clin. Invest. 76:1147-1154. McManus, I.C. 1983. Bimodality of blood pressure levels. Stat. Med. 2:253-258. Medeiros, D.M., and LK. Pellum. 1984. Elevation of cadmium, lead, and zinc in the hair of adult black female hypertensives. Bull. Environ. Contam. Toxicol. 32:525-532. Meneely, G.R., and C.O. Ball. 1958. Experimental epidemiology of chronic sodium chloride toxicity and the protective effect of potassium chloride. Am. J. Med. 25:713-725. Miller, J.Z., and C.E. Grim. 1983. Heritability of blood pressure. Pp. 79-90 in T.A. Kotchen and J.M. Kotchen, eds. Clinical Approaches to High Blood Pressure in the Young. John Wright, Boston. Morino, T., R. McCaa, and H.G. Langford. 1978. Effect of potassium loading on blood pressure, sodium excretion and plasma renin activity in hypertensive patients. Clin. Res. 26:805a. Moritz, V., P. Singer, D. Förster, I. Berger, and S. Massow. 1985. Changes of blood pressure in spontaneously hypertensive rats dependent on the quantity and quality of fat intake. Biomed. Biochim. Acta 44:1491-1505. Muirhead, E.E., B.E. Leach, J.O. Davis, F.B. Armstrong, J.A. Pitcock, and W.L.S. Brosius. 1975. Pathophysiology of angiotensin-salt hypertension. J. Lab. Clin. Med. 85:734-745. Oberman, A., N.E. Lane, W.R. Harlan, A. Graybiel, and R.E. Mitchell. 1967. Trends in systolic blood pressure in the thousand aviator cohort over a twenty-four-year period. Circulation 36:812-822. Okamoto, K., and K. Aoki. 1963. Development of a strain of spontaneously hypertensive rats. Jpn. Circ. J. 27:282-293. Ophir, O., G. Peer, J. Gilad, M. Blum, and A. Aviram. 1983. Low blood pressure in vegetarians: the possible role of potassium. Am. J. Clin. Nutr. 37:755-762. Page, L.B. 1979. Hypertension and atherosclerosis in primitive and acculturating societies. Pp. 1-12 in J.C. Hunt, ed. Hypertension Update, Vol. 1. Health Learning Systems, Lyndhurst, N.J. Page, L.B., and J. Friedlaender. 1986. Blood pressure, age and cultural change: a longitudinal study of Solomon Islands populations. Pp. 11-26 in M.J. Horan, G.M. Steinberg, J.B. Dunbar, and E.C. Hadley, eds. NIH Workshop on Blood Pressure Regulation and Aging: Proceedings from a Symposium. Biomedical Information Corp., New York. Page, L.B., A. Damon, and R.C. Moellering, Jr. 1974. Antecedents of cardiovascular disease in six Solomon Islands societies. Circulation 49:1132-1146. Page, L.B., D.E. Vandevert, K. Nader, N.K. Lubin, and J.R. Page. 1981. Blood pressure of Qash'qai pastoral nomads in Iran in relation to culture, diet, and body form. Am. J. Clin. Nutr. 34:527-538. Perry, H.M., Jr., and S.J. Kopp. 1983. Does cadmium contribute to human hypertension? Sci. Total Environ. 26:223-232. Platt, R. 1947. Heredity in hypertension. Q. J. Med. 16:111-133. Poulter, N.R., K.T. Khaw, M. Mugambi, W.S. Peart, and P.S. Sever. 1985. Migration-induced changes in blood pressure: a controlled longitudinal study. Clin. Exp. Pharmacol. Physiol. 12:211-216. Prineas, R.J., and H. Blackburn. 1985. Clinical and epidemiologic relationships between electrolytes and hypertension. Pp. 63-85 in M.J. Horan, M. Blaustein, J.B. Dunbar, W. Kachadorian, N.M. Kaplan, and A.P. Simopoulos, eds. NIH Workshop on Nutrition and Hypertension: Proceedings from a Symposium. Biomedical Information Corp., New York. Prior, I.A.M., A. Hooper, J. Huntsman, J.M Stanhope, and C.E. Salmond. 1977. The Tokelau Island migrant study. Pp. 165-186 in G.A. Harrison, ed. Population Structure and Human Variation. Cambridge University Press, London. Puska, P., J.M. Iacono, A. Nissinen, H.J. Korhonen, E. Vartiainen, P. Pietinen, R. Dougherty, U. Leino, M. Mutanen, S. Moisio, and J. Huttunen. 1983. Controlled randomised trial of the effect of dietary fat on blood pressure. Lancet 1:1-5. Reed, D., D. McGee, K. Yano, and J. Hankin. 1985. Diet, blood pressure, and multicollinearity. Hypertension 7:405-410. Reisin, E., R. Abel, M. Modan, D.S. Silverberg, H.E. Eliahou, and B. Modan. 1978. Effect of weight loss without salt restriction on the reduction of blood pressure in overweight hypertensive patients. N. Engl. J. Med. 298:1-6. Resnick, LM., J.P. Nicholson, and J.H. Laragh. 1984. Outpatient therapy of essential hypertension with dietary calcium supplementation. J. Am. Coll. Cardiol. 3:616. Rostand, S.G., K.A. Kirk, E.A. Rutsky, and B.A. Pate. 1982. Racial differences in the incidence of treatment for endstage renal disease. N. Engl. J. Med. 306:1276-1279.
OCR for page 560
Page 560 Rouse, I.L., B.K. Armstrong, and L.J. Beilin. 1982. Vegetarian diet, lifestyle and blood pressure in two religious populations. Clin. Exp. Pharmacol. Physiol. 9:327-330. Rouse, I.L., L.J. Beilin, B.K. Armstrong, and R. Vandongen. 1983. Blood-pressure-lowering effect of a vegetarian diet: controlled trial in normotensive subjects. Lancer 1:5-10. Rouse, I.L., and L.J. Beilin. 1984. Vegetarian diet and blood pressure. J. Hypertens. 2:231-240. Sacks, F.M., B. Rosner, and E.H. Kass. 1974. Blood pressure in vegetarians. Am. J. Epidemiol. 100:390-398. Schacter, J., L.H. Kuller, and C. Perfetti. 1982. Blood pressure during the first two years of life. Am. J. Epidemiol. 116:29-41. Schlierf, G., L. Arab, B. Schellenberg, P. Oster, R. Mordasini, H. Schmidt-Gayk, and G. Vogel. 1980. Salt and hypertension: data from the "Heidelberg Study." Am. J. Clin. Nutr. 33:872-875. Sever, P.S., D. Gordon, W.S Peart, and P. Beighton. 1980. Blood-pressure and its correlates in urban and tribal Africa. Lancet 2:60-64. Simpson, F.O. 1985. Blood pressure and sodium intake. Pp. 175-190 in C.J. Bulpitt, ed. Handbook of Hypertension, Vol. 6. The Epidemiology of Hypertension. Elsevier Science Publ., New York. Singer, D.R.J., N.D. Markandu, F.P. Cappucio, G.W. Beynon, A.C. Shore, S.J. Smith, and G.A. MacGregor. 1985. Does oral calcium lower blood pressure: a double-blind study. J. Hypertension 3:661. Society of Actuaries. 1959. Build and Blood Pressure Study, Vol 1. Society of Actuaries, Chicago. 268 pp. Stamler, J., D.M. Berkson, A. Dyer, M.H. Lepper, H.A. Lindberg, O. Paul, H. McKean, P. Rhomberg, J.A. Schoenberger, R.B. Shekelle, and R. Stamler. 1975. Relationship of multiple variables to blood pressurefindings from four Chicago epidemiologic studies. Pp. 307-356 in O. Paul, ed. Epidemiology and Control of Hypertension. Stratton Intercontinental Medical Book Co., New York. Stamler, J., E. Farinaro, L.M. Mojonnier, Y. Hall, D. Moss, and R. Stamler. 1980. Prevention and control of hypertension by nutritional-hygienic means. Long-term experience of the Chicago Coronary Prevention Evaluation Program. J. Am. Med. Assoc. 243:1819-1823. Svetkey, L.P., W.E. Yarger, J.R. Feussner, E. DeLong, and P.E. Klotman. 1986. Placebo-controlled trial of oral potassium in the treatment of mild hypertension. Clin. Res. 34:487a. Tao, S.C., R.S. Tsai, Z.G. Hong, and J. Stamler. 1984. Timed overnight sodium and potassium excretion and blood pressure in steel workers in Peoples' Republic of China, (PRC)-North. CVD Epidemiol. Newsletter (AHA) 35:64. Taylor, J.R., T. Combs-Orme, D. Anderson, D.A. Taylor, and C. Koppenol. 1984. Alcohol, hypertension, and stroke. Alcoholism 8:283-286. Tobian, L 1983. Human essential hypertension: implications of animal studies. Ann. Intern. Med. 98:729-734. Tobian, L 1986. High potassium diets markedly protect against stroke deaths and kidney disease in hypertensive rats, a possible legacy from prehistoric times. Can. J. Physiol. Pharmacol. 64:840-848. Tobian, L., J. Lange, S. Azar, J. Iwai, D. Koop, and K. Coffee. 1977. Reduction of intrinsic natriuretic capacity in kidneys of Dahl hypertension-prone rats. Trans. Assoc. Am. Physicians 90:401-406. Tobian, L, D. MacNeill, M.A. Johnson, M.C. Ganguli, and J. Iwai. 1984. Potassium protection against lesions of the renal tubules, arteries, and glomeruli and nephron loss in salt-loaded hypertensive Dahl S rats. Hypertension 6: 1170-1176. Tobian, L., J. Lange, K. Ulm, L. Wold, and J. Iwai. 1985. Potassium reduces cerebral hemorrhage and death rate in hypertensive rats, even when blood pressure is not lowered. Hypertension 7:1110-1114. Tobian, L, T. Sugimoto, M.A. Johnson, and S. Hanlon. 1987. High K diets protect against hypertensive intimal lesions and endothelial injury in arteries of stroke-prone hypertensive rats. Trans. Assoc. Am. Physicians 100:300-304. Trowell, H. 1981. Hypertension, obesity, diabetes mellitus and coronary heart disease. Pp. 3-32 in H.C. Trowell and D.P. Burkitt, eds. Western Diseases: Their Emergence and Prevention. Edward Arnold, London. Tuck, M.L., J. Sowers, L. Dornfeld, G. Kledzik, and M. Maxwell. 1981. The effect of weight reduction on blood pressure, plasma renin activity, and plasma aldosterone levels in obese patients. N. Engl. J. Med. 304:930-933. Tyroler, H.A., S. Heyden, and C.G. Hames. 1975. Weight and hypertension: Evans County studies of blacks and whites. Pp. 177-204 in O. Paul, ed. Epidemiology and Control of Hypertension. Stratton Intercontinental Medical Book Co., New York. Ueshima, H., T. Ogihara, S. Baba, Y. Tabuchi, K. Mikawa, K. Hashizume, T. Mandai, H. Ozawa, Y. Kumahara, S. Asakura, and M. Hisanari. 1987. The effect of reduced alcohol consumption on blood pressure: a randomised, controlled, single blind study. J. Hum. Hypertens. 1:113-119. Urata, H., Y. Tanabe, A. Kiyonaga, M. Ikeda, H. Tanaka, M. Shindo, and K. Arakawa. 1987. Antihypertensive and volume-depleting effects of mild exercise on essential hypertension. Hypertension 9:245-252. Viart, P. 1977. Hemodynamic findings in severe protein-calorie malnutrition. Am. J. Clin. Nutr. 30:334-348. von Arbin, M., M. Britton, U. de Faire, and A. Tisell. 1985. Circulatory manifestations and risk factors in patients with acute cerebrovascular disease and in matched controls. Acta Med. Scand. 218:373-380. Voors, A.W., E.R. Dalferes, Jr., G.C. Frank, G.G. Aristimuno, and G.S. Berenson. 1983. Relation between ingested potassium and sodium balance in young blacks and whites. Am. J. Clin. Nutr. 37:583-594. Walker, W.G., P.K. Whelton, H. Saito, R.P. Russell, and J. Hermann. 1979. Relation between blood pressure and renin, renin substrate, angiotensin II, aldosterone and urinary sodium and potassium in 574 ambulatory subjects. Hypertension 1:287-291. Watt, G.C., C.J. Foy, and J.T. Hart. 1983. Comparison of blood pressure, sodium intake, and other variables in offspring with and without a family history of high blood pressure. Lancet 1:1245-1248. Weinberger, M.H., J.Z Miller, F.C. Luft, C.E. Grim, and N.S. Fineberg. 1986. Definitions and characteristics of sodium sensitivity and blood pressure resistance. Hypertension 8:II127-II134. Whanger, P.D. 1979. Cadmium effects in rats on tissue iron, selenium, and blood pressure; blood and hair cadmium in some Oregon residents. Environ. Health Perspect. 28:115-121. Whitescarver, S.A., C.E. Ott, B.A. Jackson, G.P. Guthrie, Jr., and T.A. Kotchen. 1984. Salt-sensitive hypertension:
OCR for page 561
Page 561 contribution of chloride. Science 223:1430-1432. Wilczynski, E.A., and F.H. Leenen. 1987. Dietary sodium intake and age in spontaneously hypertensive rats: effects on blood pressure and sympathetic activity. Life Sci. 41:707- 715. WHO (World Health Organization). 1978. Arterial Hypertension. Report of a WHO Expert Committee. Technical Report Series 628. World Health Organization, Geneva. 58 pp. Working Group on Risk and High Blood Pressure. 1985. An epidemiological approach to describing risk associated with blood pressure levels. Hypertension 7:641-651. Zinner, S.H., P.S. Levy, and E.H. Kass. 1971. Familial aggregation of blood pressure in childhood. N. Engl. J. Med. 284:401-404.
OCR for page 562
Representative terms from entire chapter: