that leads to secondary renal damage and cardiovascular remodeling, including diminished endothelium-dependent arterial dilation to reactive hyperemia (Snieder et al., 2002). Another manifestation of vascular remodeling is increased arterial stiffness which in turn is associated with stroke, renal failure, and coronary artery disease and left ventricular hypertrophy, which is a strong predictor of cardiovascular morbidity and mortality (Snieder et al., 2002).
Snieder et al. (2002) also examined the evidence for the role of specific candidate genes on cardiovascular response to stress. Since the β2-adrenergic receptor mediates peripheral vasodilation, polymorphic variation in this gene may influence response to stress. Evidence has been provided for an association between Arg16Gly polymorphism β2-adrenergic receptor gene (ADRB2) and the Arg389Gly and Arg16Gly polymorphisms in the β1-adrenergic receptor gene (ADRB1) were associated with blood pressure at rest and reactivity to stress. The Gln27Glu polymorphism of the β2-adrenergic receptor gene also showed significantly higher levels of blood pressure at rest and stress but interestingly, no associations were found between these polymorphisms and cardiovascular reactivity for African Americans (Snieder et al., 2002). It should also be noted that an increase in cardiovascular response to stress has also been associated with a promoter polymorphism of the serotonin transporter gene (5HTTLPR) through higher levels of serotonin (Williams et al., 2001).
Snieder et al. (2002) suggested that future studies investigating genetic influences on cardiovascular and renal stress should employ measures of polymorphic variation in candidate genes that underlie the SNS, the ES, and the RAAS. They argue that rather than studying the effects of candidate genes in isolation that the biobehavioral model provides a framework for describing the interrelated physiological network underlying blood pressure regulation in response to stress. More specifically, Snieder et al. (2002) suggest the following candidate genes for the respective systems. SNS: “the α1- and α2-adrenergic receptor gene (ADRA1, ADRA2) and the β1- and β2-adrenergic receptor genes (ADRB1, ADRB2)”; RAAS: “the genes for angiotensin converting enzyme, and the angiotensin II type-1 receptor (AGTR1), aldosterone synthase (CYP11B2) and angiotensinogen”; ES: “the ET-1 gene (EDN1), the gene for ET-1 receptor A (EDNRA) and the genes for the three types of nitric oxide synthase (NOS1, NOS2, NOS3)” (Snieder et al., 2002, p. 87).
This review provides some information with regard to the specific questions of interest but may have its most significant contribution in terms of guidance of future research. In terms of what knowledge/data we have, the following findings are most salient: