The many targets of aldosterone.
The many targets of aldosterone.
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醛固酮的许多靶标。
DOI：
10.1161/01.hyp.0000123573.60340.9b
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发表时间：
2004
期刊：
影响因子：
8.3
通讯作者：
E. Schiffrin
中科院分区：
文献类型：
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作者：
E. Schiffrin
在最新一期的《高血压》中，Oberleithner等人1证明了醛固酮通过盐皮质激素受体刺激水进入人内皮细胞的新作用。使用原子力显微镜，这些作者表明，培养的人脐静脉内皮细胞响应醛固酮与钠和水的进入（他们膨胀），这可以被盐皮质激素受体阻滞剂（螺内酯）。当应用微摩尔浓度的阿米洛利时，Swedish醛固酮处理的内皮细胞收缩，在该浓度下阿米洛利不抑制钠质子交换剂。作者报告说，他们已经表明，cariporide，钠质子交换的选择性抑制剂，不影响醛固酮诱导的内皮细胞肿胀。1因此，他们认为阿米洛利抑制钠通道类似于远端肾单位的顶端上皮钠通道。作者得出结论，钠通道是由醛固酮的基因组效应诱导的，这导致钠内流和细胞去极化，产生电化学梯度，导致氯和水积聚和细胞肿胀。阿米洛利通过阻断钠通道使细胞超极化，导致氯流出，随后是水流出和细胞收缩。这种解释是否正确还有待证明。作者提出，内皮细胞肿胀后，钠内流也导致激活钠/钾ATP酶和钾内流。他们认为，考虑到内皮细胞的巨大表面积，醛固酮不仅可以通过其肾脏作用降低血清钾浓度，而且还可以通过诱导钾分泌介导。
In the current issue of Hypertension , Oberleithner et al1 demonstrate a new effect of aldosterone acting via mineralocorticoid receptors to stimulate water entry into human endothelial cells. Using atomic force microscopy, these authors show that cultured human umbilical vein endothelial cells respond to aldosterone with sodium and water entry (they swell) and this can be blocked by a mineralocorticoid receptor blocker (spironolactone). Swollen aldosterone-treated endothelial cells shrink when micromolar concentrations of amiloride are applied, concentrations at which amiloride does not inhibit the sodium-proton exchanger. The authors report they already showed that cariporide, a selective inhibitor of the sodium-proton exchanger, does not affect aldosterone-induced endothelial cell swelling.1 Thus, they suggest that amiloride inhibits a sodium channel similar to the apical epithelial sodium channel in the distal nephron. The authors conclude that sodium channels are induced by genomic effects of aldosterone, which result in sodium influx and cell depolarization, creating an electrochemical gradient that leads to chloride and water accumulation and cell swelling. Amiloride, by blocking the sodium channels, hyperpolarizes the cell, leading to chloride efflux followed by efflux of water and cell shrinkage. Whether this interpretation is correct remains to be proven. The authors propose that endothelial cell swelling followed by sodium influx also leads to activation of the sodium/potassium ATPase and potassium influx. They suggest that, considering the huge surface of endothelium, aldosterone may reduce serum concentrations of potassium not only by its renal action but also mediated by inducing potassium …
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