Bia J M, Tyler K, DeFronzo R A
Endocrinology. 1982 Sep;111(3):882-8. doi: 10.1210/endo-111-3-882.
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 micrograms/100 g BW) dexamethasone injection produced a 70% increase in urinary potassium (K) excretion (0.99 +/- 0.06 to 1.70 +/- 0.20 mueq/min; P less than 0.005) but had no effect on sodium excretion. In contrast, low doses of aldosterone (2.5 micrograms/100 g BW) caused a significant decrease in urinary sodium excretion (6.23 +/- 1.2 to 2.75 +/- 0.7 mueq/min; P less than 0.01) but had no influence on renal potassium excretion (UKV). Higher doses of dexamethasone (10, 20 and 50 micrograms/100 g BW) produced a greater kaliuresis, increasing UKV by more than 100% over baseline and higher (P less than 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.
研究了低剂量和高剂量地塞米松对长期（2 - 3周）肾上腺切除大鼠肾脏电解质排泄的急性影响，并与醛固酮的影响进行了比较。在地塞米松最低有效剂量（2微克/100克体重）注射后，尿钾（K）排泄增加了70%（从0.99±0.06增加到1.70±0.20微当量/分钟；P<0.005），但对钠排泄无影响。相比之下，低剂量醛固酮（2.5微克/100克体重）导致尿钠排泄显著减少（从6.23±1.2减少到2.75±0.7微当量/分钟；P<0.01），但对肾脏钾排泄（UKV）无影响。更高剂量的地塞米松（10、20和50微克/100克体重）产生了更大的尿钾增多效应，使UKV比基线增加超过100%，且高于低剂量地塞米松后的数值（P<0.05），但同样未能降低钠排泄。所有剂量地塞米松后UKV的增加都伴随着尿钾浓度的显著增加；在更高剂量地塞米松时，尿量有不同程度的增加。UKV的增加并非继发于血浆钾浓度的升高，也与地塞米松给药后血压或肾小球滤过率的升高无关。这些发现表明，在肾上腺切除的大鼠中，急性给予低剂量和高剂量地塞米松可增加尿钾排泄而不影响钠排泄。相比之下，醛固酮对钾排泄影响很小，但显著降低钠排泄。这些结果表明，地塞米松后观察到的尿钾增多不能归因于该激素的盐皮质激素特性。
