Glucocorticoid effects on Na-K-ATPase in rabbit nephron segments.
Glucocorticoid effects on Na-K-ATPase in rabbit nephron segments.
复制标题
糖皮质激素对兔肾单位 Na-K-ATP 酶的影响。
作者：
L. Garg;N. Narang;C. Wingo
本文观察了地塞米松对肾上腺切除家兔六个肾单位钠-钾-ATP酶活性的影响。在研究肾单位节段之前，治疗包括1.4 μ g地塞米松X 100 g体重-1 X天-1，持续7天。通过显微荧光测定法测定单个肾单位节段中的酶活性。与对照组（假手术组）相比，肾上腺切除组家兔近曲小管S1段（PCT，S1）、髓质粗升支（MTAL）和远曲小管（DCT）的Na-K-ATP酶活性降低40-50%。肾上腺切除组和对照组动物近端直小管（PST、S2和S3）和皮质粗升支（CTAL）中的酶活性无显著差异。地塞米松处理在血浆中产生5 +/- 0.8 nM的地塞米松浓度，并将肾上腺切除动物的PCT（S1）、MTAL和DCT中的Na-K-ATP酶活性增加至对照水平，而不会显著影响PST（S2，S3）或CTAL中的酶活性。地塞米松在血浆中的浓度应使激素主要与地塞米松受体结合（Kd = 5 nM），与醛固酮受体结合很少（Kd大于60 nM）。因此，糖皮质激素可能通过糖皮质激素（II型）受体而不是盐皮质激素（I型）受体刺激PCT、MTAL和DCT中的Na-K-ATP酶。
We determined the effect of dexamethasone on Na-K-ATPase activity in six nephron segments of the adrenalectomized rabbit. Treatment consisted of 1.4 micrograms dexamethasone X 100 g body wt-1 X day-1 for 7 days prior to the study of the nephron segments. Enzyme activity was determined in individual nephron segments by a microfluorometric assay. There was 40-50% less activity of Na-K-ATPase in the S1 portion of the proximal convoluted tubule (PCT, S1), the medullary thick ascending limb (MTAL), and the distal convoluted tubule (DCT) of adrenalectomized rabbits compared with that of control (sham-operated) animals. There was no significant difference in the enzyme activity in proximal straight tubules (PST, S2 and S3) and cortical thick ascending limb (CTAL) of adrenalectomized and control animals. Dexamethasone treatment produced a dexamethasone concentration of 5 +/- 0.8 nM in the plasma and increased Na-K-ATPase activity in PCT (S1), MTAL, and DCT of the adrenalectomized animals to the control levels without significantly affecting the enzyme activity in the PST (S2, S3) or CTAL. The concentration of dexamethasone in the plasma was such that the hormone should bind mainly to dexamethasone receptors (Kd = 5 nM) and very little to aldosterone receptors (Kd greater than 60 nM). Thus, glucocorticoids probably stimulate Na-K-ATPase in PCT, MTAL, and DCT through glucocorticoid (Type II) receptors and not through mineralocorticoid (Type I) receptors.