Regulation of renal Na+-K+-ATPase in the rat by adrenal steroids.
Regulation of renal Na+-K+-ATPase in the rat by adrenal steroids.
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肾上腺类固醇对大鼠肾 Na -K -ATP 酶的调节。
DOI：
10.1152/ajprenal.1981.241.2.f186
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Klahr,S
中科院分区：
文献类型：
--
作者：
Rodriguez,HJ;Sinha,SK;Starling,J;Klahr,S
在肾上腺切除大鼠模型上，观察了单次和多次注射醛固酮和地塞米松对肾脏Na ~+-K ~+-ATP酶、离体肾脏再生和尿电解质排泄的影响，并呈剂量依赖性。单次最大和超大剂量的醛固酮（根据电解质排泄的影响确定）对Na+-K+-ATP酶或血管生成没有影响。相比之下，单次给予地塞米松（剂量范围增加空腹血糖，刺激肾脏新生，没有盐皮质激素作用）产生明显的Na+-K+-ATP酶激活。多次亚最大剂量地塞米松产生的Na+-K+-ATP酶和神经再生的刺激在数量上相似。多个超大剂量的醛固酮刺激Na+-K+-ATP酶和血管生成，但最大和次大剂量的激素没有影响。醛固酮对肝Na ~+-K ~+-ATP酶活性及肝细胞再生无影响。这些结果表明，肾Na+-K+-ATP酶的激活可以被认为是一种假定的糖皮质激素（而不是盐皮质激素）的作用。慢性醛固酮治疗引起的肾Na+-K+-ATP酶激活可能是由糖皮质激素受体位点介导的，因此可能不代表真正的盐皮质激素效应。
The effects of single and multiple injections of aldosterone and dexamethasone on renal Na+-K+-ATPase, in vitro renal gluconeogenesis, and urinary electrolyte excretion were examined in adrenalectomized rats in a dose-dependent manner. Single maximal and supramaximal doses of aldosterone (defined by the effect of electrolyte excretion) had no effect on Na+-K+-ATPase or gluconeogenesis. By contrast, a single administration of dexamethasone (in a dose range that increased fasting blood sugar, stimulated renal gluconeogenesis, and had no mineralocorticoid effects) yielded clear-cut activation of Na+-K+-ATPase. Multiple submaximal doses of dexamethasone produced quantitatively similar stimulation of Na+-K+-ATPase and gluconeogenesis. Multiple supramaximal doses of aldosterone stimulated Na+-K+-ATPase and gluconeogenesis, but maximal and submaximal doses of the hormone were without effect. Aldosterone had no effect on hepatic Na+-K+-ATPase or gluconeogenesis. These results suggest that activation of renal Na+-K+-ATPase can be considered a putative glucocorticoid (not mineralocorticoid) effect. Renal Na+-K+-ATPase activation by chronic aldosterone treatment may be mediated by glucocorticoid receptor sites and, hence, may not represent a genuine mineralocorticoid effect.