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Research Article Free access | 10.1172/JCI105561

Role of the Sympathetic Nervous System in Regulating Renin and Aldosterone Production in Man

Richard D. Gordon, Oto Küchel, Grant W. Liddle, and Donald P. Island

Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn.

†

Address requests for reprints to Dr. Grant W. Liddle, Dept. of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn. 37203.

*

Submitted for publication July 19, 1966; accepted December 22, 1966.

These studies were supported in part by the following grants-in-aid from the National Institutes of Health: 5-K6-AM-3782, 8MOI-FR-95, TI-AM-5092, and 5-ROI-AM-05318.

Find articles by Gordon, R. in: JCI | PubMed | Google Scholar

Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn.

†

Address requests for reprints to Dr. Grant W. Liddle, Dept. of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn. 37203.

*

Submitted for publication July 19, 1966; accepted December 22, 1966.

These studies were supported in part by the following grants-in-aid from the National Institutes of Health: 5-K6-AM-3782, 8MOI-FR-95, TI-AM-5092, and 5-ROI-AM-05318.

Find articles by Küchel, O. in: JCI | PubMed | Google Scholar

Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn.

†

Address requests for reprints to Dr. Grant W. Liddle, Dept. of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn. 37203.

*

Submitted for publication July 19, 1966; accepted December 22, 1966.

These studies were supported in part by the following grants-in-aid from the National Institutes of Health: 5-K6-AM-3782, 8MOI-FR-95, TI-AM-5092, and 5-ROI-AM-05318.

Find articles by Liddle, G. in: JCI | PubMed | Google Scholar

Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn.

†

Address requests for reprints to Dr. Grant W. Liddle, Dept. of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn. 37203.

*

Submitted for publication July 19, 1966; accepted December 22, 1966.

These studies were supported in part by the following grants-in-aid from the National Institutes of Health: 5-K6-AM-3782, 8MOI-FR-95, TI-AM-5092, and 5-ROI-AM-05318.

Find articles by Island, D. in: JCI | PubMed | Google Scholar

Published April 1, 1967 - More info

Published in Volume 46, Issue 4 on April 1, 1967
J Clin Invest. 1967;46(4):599–605. https://doi.org/10.1172/JCI105561.
© 1967 The American Society for Clinical Investigation
Published April 1, 1967 - Version history
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Abstract

Several lines of evidence have been developed indicating that the sympathetic nervous system may play a role in mediating the renal and adrenocortical secretory 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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