The acute effect of low and high doses of dexamethasone on renal electrolyte excretion was examined in chronically (2-3 weeks) adrenalectomized rats and was compared with that of aldosterone. At the lowest effective dose (2 μg/100 g BW) dexamethasone injection produced a 70% increase in urinary potassium (K) excretion (0.99 ± 0.06 to 1.70 ± 0.20 μeq/min; P < 0.005) but had no effect on sodium excretion. In contrast, low doses of aldosterone (2.5 μg/100 g BW) caused a significant decrease in urinary sodium excretion (6.23 ± 1.2 to 2.75 ± 0.7 μeq/min; P < 0.01) but had no influence on renal potassium excretion (UKV). Higher doses of dexamethasone (10, 20, and 50 μg/100 g BW) produced a greater kaliuresis, increasing UKV by more than 100% over baseline and higher (P < 0.05) than values after a low dose of dexamethasone, but again failed to lower sodium excretion. The increase in UKV after all doses of dexamethasone occurred in association with a significant increase in urinary K concentration; at higher doses of dexamethasone there was a variable increase in urine flow. The increase in UKV was not secondary to an increase in plasma K concentration nor was it associated with a rise in blood pressure or glomerular filtration rate after dexamethasone administration. These findings demonstrate that, in the adrenalectomized rat, acute administration of low and high doses of dexamethasone increases urinary K excretion without affecting sodium excretion. In contrast, aldosterone has little effect on K excretion but significantly decreases sodium excretion. These results indicate that the kaliuresis observed after dexamethasone cannot be attributed to a mineralocorticoid property of the hormone.
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