Mechanisms regulating aldosterone secretion during sodium depletion

Abstract

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.

Sites of action of sodium depletion on aldosterone biosynthesis in the dog

“…The secretion rates of aldosterone and of corticosterone in the sodium-depleted dogs are 10-fold, that of cortisol is fivefold, the rates in sodium-replete dogs. This pattern of steroid secretion is similar to that seen after administration of renin or angiotensin in vivo (7)(8)(9)(10), and is in agreement with previous data from the sodiumdepleted dog ( 11,12).…”

Studies of the control of plasma aldosterone concentration in normal man

“…Alterations of aldosterone secretion in response to sodium restriction, posture, acute diuresis, or hemorrhage have been widely considered to be mediated by the reninangiotensin system (1)(2)(3)(4). Other factors, such as potassium (5-7), adrenocorticotropin (ACTH) (7)(8)(9), and serotonin (10) have been shown to alter aldosterone secretion in vivo and/or in vitro, but presumably, they play only a minor role in comparison to the renin-angiotensin system in controlling the secretion of aldosterone in response to volume changes.…”

“…The Journal of Clinical Investigation Volume 51 July 1972urinary excretion or secretion rates of aldosterone determined over hours to single or multiple but instantaneous determinations of renin activity or angiotensin II levels (3,4,6,8,14). The exact relationship of renin activity to plasma aldosterone when changes in volume are produced have not been entirely clear fromn the few previous studies when both have been measured simultaneously (13, 15,16) and none have measured both potassium and ACTH levels, directly or indirectly, at the same time.…”

The biosynthesis of adrenal steroids: effects of angiotensin II, adrenocorticotropin, and potassium.

“…Despite a large number of in vivo experiments involving ,the rat, dog, sheep, and man, the exact locus of each stimulus within the control mechanism and the precise relationships of one to the other have not been clearly defined. In particular, disagreement persists as to the physiologic role of the renin-angiotensin system (2,3,5).The initial results of in vitro studies of the effects of ACTH and angiotensin on the biosynthesis of adrenal steroids have been published (6). In those studies, in which the effects upon aldosterone and cortisol were nonselective, relatively large amounts of both agents were used.…”

“…All three have been shown to stimulate the production of aldosterone in the intact animal (1)(2)(3)(4). Despite a large number of in vivo experiments involving ,the rat, dog, sheep, and man, the exact locus of each stimulus within the control mechanism and the precise relationships of one to the other have not been clearly defined.…”