Renal intercalated cells and blood pressure regulation.
Renal intercalated cells and blood pressure regulation.
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DOI：
10.23876/j.krcp.2017.36.4.305
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发表时间：
2017-12
影响因子：
3
通讯作者：
Wall SM
中科院分区：
文献类型：
--
作者：
Wall SM
B型和非A型、非B型闰间细胞见于连接小管和皮质集合管。在这些细胞类型中，已知B型插入细胞主要通过pendrine依赖的Cl−/HCO 3 −交换来介导Cl−吸收和HCO 3 −分泌。这种交换受到血管紧张素II给药的刺激，并且在代谢性前列腺增生模型中也受到刺激，例如在醛固酮或NaHCO 3给药后。在一些啮齿动物模型中，pendrine介导的HCO 3 −分泌调节酸碱平衡。然而，pendrin在血压调节中的作用可能更具生理或临床意义。Pendrin不仅通过介导醛固酮敏感性Cl−吸收来调节血压，还通过调节醛固酮对上皮Na+通道（ENaC）介导的Na+吸收的反应来调节血压。Pendrin通过改变开放通道的概率、通道表面密度和通道亚基总蛋白丰度来调节ENaC。因此，醛固酮通过直接和间接作用刺激ENaC活性，后者通过刺激pendrin表达和功能而发生。因此，pendrin有助于醛固酮升压反应。Pendrin也可以通过其在肾上腺髓质中的作用部分地调节血压，在肾上腺髓质中它调节儿茶酚胺的释放，或者通过对血管收缩力的间接作用。本文综述了醛固酮和血管紧张素II诱导的信号传导如何调节pendrin以及pendrin在远端肾单位功能和血压中的作用。
Type B and non-A, non-B intercalated cells are found within the connecting tubule and the cortical collecting duct. Of these cell types, type B intercalated cells are known to mediate Cl− absorption and HCO3− secretion largely through pendrin-dependent Cl−/HCO3− exchange. This exchange is stimulated by angiotensin II administration and is also stimulated in models of metabolic alkalosis, for instance after aldosterone or NaHCO3 administration. In some rodent models, pendrin-mediated HCO3− secretion modulates acid-base balance. However, the role of pendrin in blood pressure regulation is likely of more physiological or clinical significance. Pendrin regulates blood pressure not only by mediating aldosterone-sensitive Cl− absorption, but also by modulating the aldosterone response for epithelial Na+ channel (ENaC)-mediated Na+ absorption. Pendrin regulates ENaC through changes in open channel of probability, channel surface density, and channels subunit total protein abundance. Thus, aldosterone stimulates ENaC activity through both direct and indirect effects, the latter occurring through its stimulation of pendrin expression and function. Therefore, pendrin contributes to the aldosterone pressor response. Pendrin may also modulate blood pressure in part through its action in the adrenal medulla, where it modulates the release of catecholamines, or through an indirect effect on vascular contractile force. This review describes how aldosterone and angiotensin II-induced signaling regulate pendrin and the contributory role of pendrin in distal nephron function and blood pressure.