Mechanisms regulating aldosterone secretion during sodium depletion

¹ Section on Experimental Cardiovascular Disease, Laboratory of Kidney and Electrolyte Metabolism, National Heart Institute, Bethesda, Maryland

Steroid secretion was studied in conscious dogs before and during 4 days of Na depletion. A threefold increase in aldosterone secretion occurred but corticosterone output was unchanged. Plasma renin was markedly elevated. Plasma Na and K concentrations were unchanged until the 4th day of Na depletion at which time plasma Na was decreased and plasma K was elevated. The Na content of the adrenal cortex expressed as fat-free tissue solids was decreased. It seems likely that the adrenocortical Na loss was extracellular; adrenocortical K content was unaltered. It is suggested that the normal rate of corticosterone secretion during Na depletion is maintained by a negative corticosteroid feedback mechanism, since corticosterone output was consistently increased in Na-depleted hypophysectomized dogs. Aldosterone secretion was three times as great in the presence as in the absence of the anterior pituitary during Na depletion. It is concluded that increased activity of the renin-angiotensin system is the primary mechanism leading to hyperaldosteronism during Na depletion and that the adenohypophysis plays an important supportive role.

Note:
With the Surgical Assistance of Alfred Casper

Key Words: steroid secretion • corticosteroid feedback mechanism • peripheral plasma renin • secondary hyperaldosteronism • adrenocortical sodium and potassium

Submitted on October 7, 1964

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