Stimulation of aldosterone biosynthesis by sodium sequestration: role of angiotensin II

The role of angiotensin II in the stimulation of aldosterone biosynthesis by sodium sequestration in potassium-deficient rats was assessed by experiments involving 1-day angiotensin II infusion, converting enzyme inhibition, and bilateral nephrectomy. In intact rats, only an extremely high dose of exogenous angiotensin II imitated the stimulatory effects of polyethylene glycol-induced edema on the conversions of deoxycorticosterone and corticosterone to 18-hydroxycorticosterone and aldosterone. Treatment with the converting enzyme inhibitor captopril as well as bilateral nephrectomy blocked the aldosterone-stimulating action of edema. This inhibition was prevented by the simultaneous infusion of angiotensin II in captopril-treated rats but not in nephrectomized animals. According to these results, angiotensin II is an essential mediator in the stimulation of aldosterone biosynthesis by sodium sequestration. However, the role of the kidneys appears to be twofold. First, they act through the secretion of renin. In addition, a second yet unknown kidney factor is necessary for a full response of the zona glomerulosa to the stimulatory action of angiotensin II.

Stimulation of aldosterone biosynthesis by experimental edema: role of the kidneys

The role of the kidneys in the stimulation of aldosterone biosynthesis by sodium sequestration was investigated in potassium-depleted rats. After 2 wk on a potassium-deficient diet, rats were treated by subcutaneous injections of polyethylene glycol or formalin and were then kept on sucrose and water for 24 h. Either type of experimental edema markedly enhanced the conversions of tritiated deoxycorticosterone and corticosterone to aldosterone and 18-hydroxycorticosterone by incubated capsular portions of the adrenal glands and partially normalized the deranged pattern of endogenous corticosteroid output in response to serotonin. Bilateral nephrectomy completely blocked these effects of edema on the zona glomerulosa. When uremia was induced by bladder resection, with the kidneys left intact, edema still significantly stimulated aldosterone biosynthesis. Irrespective of increases in the plasma creatinine, the plasma potassium remained at uniformly low levels in all experimental groups of animals. According to these observations, experimental edema stimulates late steps of aldosterone biosynthesis in potassium-depleted rats by mediation of the kidneys, most likely through the renin-angiotensin system.