Summary. Several lines of evidence have been developed indicating that the sympathetic nervous system may play a role in mediating the renal and adrenocortical secretary responses to upright posture and sodium deprivation. Despite concurrent increases in arterial blood pressure, the plasma renin activity of normal subjects increased both in response to the infusion of catecholamines (norepinephrine: epinephrine, 10: 1) and in response to stimulation of the sympathetic nervous system by cold. Aldosterone excretion was also increased by catecholamine infusion. In normal subjects the stimuli of upright posture and of sodium depletion both resulted in increases in urinary catecholamines, plasma renin activity, and urinary aldosterone. A patient with severe autonomic insufficiency did not experience normal elevations of urinary catecholamines, plasma renin activity, or urinary aldosterone in response to upright posture or sodium deprivation, despite a substantial fall in arterial blood pressure. When orthostatic hypotension was prevented by infusion of catecholamines, however, increases in plasma renin activity and in aldosterone excretion were observed.We suggest that both upright posture and sodium depletion lead to decreases in effective plasma volume and increases in sympathetic nervous system activity. This increase in sympathetic activity is then responsible for an increase in renal afferent arteriolar constriction, leading to an increase in renin secretion and, ultimately, an increase in aldosterone secretion.

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A study of the secretion rate of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) in normal subjects and patients with benign essential hypertension by a double isotope dilution method showed a fivefold increase in the secretion rate of dehydroepiandrosterone (from 9.8 mg/day ± 3.1 mg/day S.D. to 52.0 mg/day ± 15.5 mg/day S.D.), and a sixfold increase of dehydroepiandrosterone sulfate in hypertensive patients (from 10.7 mg/day ± 2.9 mg/day S.D. to 60.7 mg/day ± 18.6 mg/day S.D.). This study was carried out following the administration of 14C-labelled DHEA and 3H-labelled DHEA-S and involved an initial column chromatographic separation of urinary DHEA-glucuronide and sulfate.

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