Mineralo- and glucocorticoid effects on renal excretion of electrolytes

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Abstract
The acute effects of mineralo- and glucocorticoids on urinary electrolyte excretion were studied in the conscious, acutely potassium deprived, adrenalectomized rat. Sodium, potassium, and creatinine were measured in the urine excreted from 2.5 to 5.5 h after injection of one or more of the following steroids: aldosterone (Aldo), 9-alpha fluorocortisol (FC), deoxycorticosterone (DOC), dexamethasone (Dex), and spironolactone (Spiro). The hierarchy (a) for increasing creatinine excretion was Dex>FC>Aldo>DOC>Spiro >none, a hierarchy consistent with glucocorticoid potency; and (b) for producing anti-natriuresis was Aldo>DOC≥FC ≥none=Spiro>Dex, a hierarchy consistent with mineralocorticoid potency. In contrast, the kaliuresis produced by mineralo- and glucocorticoids appears different. A “mineralocorticoid” kaliuresis is 1) elicited by anti-natriuretic doses of Aldo and FC, 2) approximately twice control UKV, 3) unrelated to changes in glomerular filtration rate (GFR), and 4) inhibited by Spiro. A “glucocorticoid” kaliuresis is 1) elicited by Dex and high doses of Aldo and FC, 2) about seven to twenty-fold greater than control UKV, 3) possibly dependent, in part, on changes in GFR, and, 4) not inhibited by Spiro. DOC was not kaliuretic at anti-natriuretic doses. The urinary Na/K ratio was an unreliable index of mineralocorticoid action.