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