A number of studies have reported the concentrations of serum or plasma sodium by level of dietary sodium intake. Changes in sodium intake can influence serum or plasma levels of sodium, but the changes are relatively small and do not lead to pathological conditions, such as hyponatremia. Studies have shown that low intakes of sodium (0.15 to 0.23 g [6 to 10 mmol]/day) do not result in hyponatremia (defined as plasma sodium levels < 135 mmol/L) in healthy nonhypertensive (Kirkendall et al., 1976; Luft et al., 1979b; Overlack et al., 1995; Roos et al., 1985) or hypertensive individuals (Kempner, 1948; Mark et al., 1975). When observed, hyponatremia is often caused by excessive sodium loss from the body, which occurs with impaired renal function, increased vasopressin release, or excessive consumption of water. Diuretic use is an infrequent cause of hyponatremia. Overall, there is little evidence of any adverse effect of low dietary sodium on serum or plasma sodium concentrations in healthy individuals.

Renin is released from the juxtaglomerular cells of the kidney in response to a perceived reduction in blood volume, blood pressure, or tubular sodium concentration. As a result, renin induces the production of angiotensin II, which stimulates renal sodium reabsorption via a direct tubular effect, as well as by increasing the production of aldosterone. In cross-sectional studies, plasma renin activity is inversely associated with sodium intake; the relationship appears to be curvilinear with the greatest rise in plasma renin activ-