Patterns of sodium excretion during sympathetic nervous system arousal.

Abstract

The purpose of this study was to examine Na + handling and regulation during 1 hour of behaviorally induced sympathetic nervous system (SNS) arousal followed by 2 hours of recovery. Two patterns of response were observed among experimental subjects, despite similar changes in blood pressure and heart rate. In one group (n=19), Na + excretion increased significantly during SNS arousal, which then decreased significantly during recovery (12-3 versus 16.0 versus 13.1 meq/hr, baseline, SNS arousal, recovery, respectively). Changes in Na + excretion were correlated with changes in creatinine clearance from baseline to SNS arousal (r=0.54) and SNS arousal to recovery (r=0.58), and were accompanied by significant increases in plasma renin activity (1.5 versus 2.0 ng/ml/hr) and aldosterone (8.5 versus 10J ng/ml/hr) from baseline to SNS arousal. Na + excretion decreased during SNS arousal in the other group of subjects (n=17) and remained below baseline levels during recovery (162 versus 12.7 versus 11.9 meq/hr). These changes were associated with significant decreases in creatinine clearance from baseline to recovery (138 versus 121 ml/min/1.73 m 2 ) and significant increases in plasma renin activity from baseline to SNS arousal (13 versus 2.2 ng/ml/hr) but not in aldosterone. Control subjects in =24) maintained baseline levels of each variable throughout the procedure. These results suggest that individuals differ in Na + handling and regulation during behavioral arousal. Decreases in Na + have been reported previously in humans and animals at risk for the development of hypertension. {Hypertension 1991;17:1156-1160) G uyton 1 has proposed that the renal-body fluid system is responsible for the long-term regulation of blood pressure (BP). Based on this model, increases in BP will cause the kidneys to increase the excretion of both salt (pressure natriuresis) and water (pressure diuresis), decreasing extracellular fluid volume and blood volume. This decreases cardiac output, which returns BP to previous levels. Conversely, decreases in BP increase Na + and water reabsorption, increasing cardiac output and returning BP to previous levels. The research of DiBona 2 and others 3 -9 is consistent with the hypothesis that the sympathetic nervous system (SNS) can influence the renal-body fluid system through direct actions on the renal tubules, changes in renal blood flow and glomerular filtration rate, and changes in plasma renin activity (PRA). PRA controls circulating levels of angiotensin II, which directly stimulates the renal tubules, and leads to the release of aldosterone, both of which promote Na + retention. The

Stress-Induced Sodium Excretion

“…3 For example, the heritability of salt sensitivity, defined as an increased BP response to high-salt intake or decrease of BP on a low-salt diet 9 has been well-documented 10–13 and heritabilities between 43% and 52% have been observed for fractional and 24-h sodium excretion. 14,15Furthermore, Light et al 16 showed that high reactors to a series of psychological stressors, with a family history of essential hypertension tended to retain sodium during the stress test period, which was later confirmed in further human 17 and animal studies. 18,19 Based on this evidence, we hypothesize that a genetic predisposition for impaired sodium handling will adversely affect the pressure-natriuresis response to stress.…”

Angiotensin II receptor blocker attenuates stress pressor response in young adult African Americans

“…The mental stress protocol was a modified version of the standard stress testing protocol we have used successfully up to this point in over 1000 subjects as described previously in both adult 25 and pediatric populations. 17,[26][27][28] The stressor was a competitive video game task played against another individual for monetary reward. On the testing day, the subjects were tested in a private room in a comfortable chair.…”

Biobehavioral Effects of Extended Salt Loading and Conflict Stress in Intact Baboons

“…For example, shockavoidance conditioning decreases renal blood flow in monkeys (Forsyth, 1971;Vatner, 1978) and decreases renal excretion of sodium and water in dogs (Koepke, 1985). In studies with humans, borderline hypertensives (Light, Koepke, Obrist, & Willis, 1983) and normotensive young adults both with (Light et al, 1983) and without (Harshfield, Pulliam, & Alpert, 1991) a family history of hypertension have exhibited reduced sodium excretion rates during laboratory stressors.…”