Minealocorticoid receptors and 11 beta-steroid dehydrogenase activity in renal principal and intercalated cells.

Minealocorticoid receptors and 11 beta-steroid dehydrogenase activity in renal principal and intercalated cells.
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肾主细胞和闰细胞中的盐皮质激素受体和 11 β-类固醇脱氢酶活性。

DOI:
10.1152/ajprenal.1994.266.1.f76
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发表时间:
1994
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Fejes-Toth,G
Fejes-Toth,G
中科院分区:
--
文献类型:
--
作者:
Naray-Fejes-Toth,A;Rusvai,E;Fejes-Toth,G

文献摘要

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相似文献

醛固酮对大脑皮层集合管有复杂的作用:它促进Na+和K+的转运,也影响H+和HCO3的转运。这些后一种作用是醛固酮对插层细胞(ICC)的直接作用,还是次要于其他电解质转运的变化,目前尚不清楚。由于特定受体的存在是类固醇直接作用的前提,而盐皮质激素受体(MR)在ICC中尚未被证实,在本研究中,我们直接测定了分离的主细胞(PC)和β-ICC中MR的密度。通过免疫解剖和荧光激活细胞分选,从兔肾皮质中获得这两种细胞类型的纯化群体。我们发现PC和β-ICC都含有大量的MR,尽管PC的受体密度高于β-ICC(6,704+/-912vs.2,181+/-388个MR位点/细胞;P<0.001)。11β-羟基类固醇脱氢酶(11β-OHSD)是一种主要存在于盐皮质激素靶细胞中的酶,其分布与MR在两种细胞中的分布相似。通过测定[~3H]皮质酮到11-脱氢皮质酮的转化率来确定11β-脱氢皮质酮的活性,在完整的PC和β-ICC中,分别为1.08+/-0.14和0.34+/-0.08fmol.min-1×1,000 cell-1(P<0.001)。11β-OHSD在两种细胞中均以NAD为辅因子。这些结果表明,β-ICC是醛固酮的潜在直接靶点,PC和β-ICC中的MR都受到11β-OHSD的保护。
Aldosterone exerts complex effects on the cortical collecting duct (CCD): it increases Na+and K+transport, and it also influences H+ and HCO3 transport. Whether these latter effects represent direct action of aldosterone on intercalated cells (ICC) or are secondary to changes in the transport of other electrolytes is unclear. Because the presence of specific receptors is the prerequisite of a direct steroid action, and mineralocorticoid receptors (MR) have not yet been demonstrated in ICC, in this study we determined the density of MR directly in isolated principal cells (PC) and beta-ICC. Purified populations of these two cell types were obtained from rabbit renal cortex by immunodissection and fluorescence-activated cell sorting. We found that both PC and beta-ICC contained a significant number of MR, although receptor density was higher in PC than in beta-ICC (6,704 +/- 912 vs. 2,181 +/- 388 MR sites/cell; P < 0.001). 11 beta-Hydroxysteroid dehydrogenase (11 beta-OHSD), an enzyme that is present predominantly in mineralocorticoid target cells, exhibited a distribution similar to that of MR in the two cell types. 11 beta-OHSD activity, determined by measuring the rate of conversion of [3H]corticosterone to 11-dehydrocorticosterone, was 1.08 +/- 0.14 and 0.34 +/- 0.08 fmol.min-1 x 1,000 cells-1 (P < 0.001) in intact PC and beta-ICC, respectively. 11 beta-OHSD in both cell types utilized NAD as cofactor. These results suggest that beta-ICC are potential direct targets of aldosterone and that MR in both PC and beta-ICC are protected by 11 beta-OHSD.