The Effect of Dexamethasone on Renal Electrolyte Excretion in the Adrenalectomized Rat

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Abstract
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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