Effects of Dietary Sodium and Potassium Intake and Acute Stimulation on Aldosterone Output by Isolated Human Adrenal Cells

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Abstract
The regulation of steroidogenesis by isolated cells prepared from human adrenal glands was assessed after crude separation into capsular (containing mainly glomerulosa cells with a 30–35% contamination of fasciculata cells) and decapsular (consisting almost entirely of zona fasciculatareticularis cells) fractions. Cortisol and corticosterone but not aldosterone were produced by the decapsulated cell preparation, ACTH (α 1-24) but not angiotensin II or potassium significantly increased cortisol production by these cells. Basal aldosterone production by the glomerulosa cell fraction increased significantly when cells were obtained from individuals who were sodium restricted (3-fold) or potassium loaded (17-fold). In addition, the conversion of corticosterone into aldosterone was significantly nificantly increased by sodium restriction (2-fold) and potassium loading (4-fold). The addition of ACTH (α 1-24) potassium or angiotensin II significantly increased aldosterone production from the glomerulosa cell fraction. Cells obtained from patients with primary aldosteronism responded similarly. Quantitatively, however, aldosterone and corticosterone production and the conversion of corticosterone into aldosterone was greater. Thus, the responses of the human adrenal cells are similar to those previously reported for rat cells. Furthermore, the effect of dietary potassium and sodium intake on the rate of conversion of corticosterone into aldosterone provides a biochemical explanation for a number of in vivo observations.