1981American Journal of Physiology-Endocrinology and MetabolismRequires access

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

Philippe Haldy, Jürg Müller

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Abstract

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.

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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.

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Available abstract

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.

Key concepts: Aldosterone, Internal medicine, Endocrinology, Stimulation, Low sodium diet, Plasma renin activity, Zona glomerulosa, Edema

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