To further investigate the relationship between salt intake and sympathetic nervous system activity, the short-and long-term effects of a low-salt diet (40 meq/day) were assessed in 10 normal subjects. Measurements of hemodynamic, hormonal, and other parameters were obtained on the day preceding institution of the low-salt diet (day 0) and on days 4, 7, 30, and 60 of the diet. Urinary sodium excretion was 178 1 0 meq/24 hr on day 0 and 31 ± 4, 38 4, 45 ± 6, and 47 + 7 meq/24 hr on days 4, 7, 30, and 60, respectively (all p < .001 compared with day 0). Blood pressure, urinary potassium, serum electrolytes, and cardiac function (as assessed by echocardiography) were not modified by the 2 month low-salt diet. Plasma renin activity and plasma aldosterone were significantly elevated above control values throughout the entire period of the low-salt diet. In contrast, plasma norepinephrine concentration increased significantly only on days 4 and 7 (from 253 ± 20 pg/ml on day 0 to 495 ± 32 pg/ml, p < .001, and 347 + 22 pg/ml, p < .05, respectively), returning to baseline at days 30 (280 ± 18 pg/ml) and 60 (262 + 18 pg/ml). Changes in plasma epinephrine paralleled those observed for norepinephrine. Similarly, resting heart rate and the blood pressure response to isometric exercise were significantly increased only on days 4 and 7 of the low-salt diet. These results suggest that sympathetic nervous system activity is enhanced only transiently during a sustained reduction in sodium intake. Circulation 72, No. 1, 47-52, 1985. IT HAS LONG been hypothesized that the level of sodium intake affects sympathetic nervous system activity both in normal and in hypertensive subjects. There have been several reports that circulating catecholamines increase during dietary sodium restriction'`8 and decrease upon sodium loading,3' 6-9 although some conflicting data exist. ' sensitivity to norepinephrine while it decreases the basal plasma concentration of norepinephrine, ' but others have found no change in renal vascular reactivity to norepinephrine during acute sodium repletion.'9 These discrepancies could be ascribed to differences in the experimental protocols used in the studies, such as differences in animal species used or clinical characteristics of the population studied (e.g., with respect to age, blood pressure) and differences in the duration and degree of the changes in salt intake.The purpose of the present study was to assess the time course of the humoral and hemodynamic responses to a moderate reduction in sodium intake, particularly as related to sympathetic nervous system activity, in a homogeneous group of normal human subjects.
MethodsTwelve normal volunteer subjects from 23 to 39 years old (mean + SEM = 35 ± 3.5 years) were enrolled in the study. As a group they had no history of serious illness and no family history of hypertension. Informed written consent was obtained from each and they took no drugs for the duration of the study. To achieve an equilibrium on a standardized diet for baseline measureme...