Regulation of Blood Pressure and Salt Balance By Pendrin-Positive Intercalated Cells: Donald Seldin Lecture 2020.

Regulation of Blood Pressure and Salt Balance By Pendrin-Positive Intercalated Cells: Donald Seldin Lecture 2020.
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DOI:
10.1161/hypertensionaha.121.16492
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发表时间:
2022-04
期刊:
Hypertension (Dallas, Tex. : 1979)
影响因子:
--
通讯作者:
Wall SM
Wall SM
中科院分区:
其他
文献类型:
--
作者:
Wall SM

文献摘要

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在连接小管和集合管中,嵌入细胞(IC)约占所有细胞的三分之一,并根据H+-ATP酶的亚细胞分布(决定其分泌H+或HCO 3-)分为A型、B型和非A非B型。B型插入细胞介导Cl−吸收和HCO 3 −分泌,这主要通过阴离子交换剂pendrin发生。Pendrin通过血管紧张素1a型受体被血管紧张素II刺激,通过盐皮质激素受体被醛固酮刺激。醛固酮刺激pendrin的表达和功能,部分是通过它产生的抑制作用。Pendrin介导的HCO 3 −分泌在代谢性水肿模型中增加,从而减弱水肿。然而,pendrin阳性IC也调节血压,至少部分是通过pendrin介导的Cl−吸收,并通过其对上皮Na+通道ENaC的间接作用。这种醛固酮诱导的pendrin增加继发性刺激ENaC,从而促进醛固酮升压反应。本文综述了pendrin阳性IC对Na+、K+、Cl−和酸碱平衡的贡献。
Intercalated cells (IC) make up about a third of all cells within the connecting tubule and the collecting duct and are subclassified as type A, type B and Non-A, non-B based on the subcellular distribution of the H+-ATPase, which dictates whether it secretes H+ or HCO3−. Type B intercalated cells mediate Cl− absorption and HCO3− secretion, which occurs largely through the anion exchanger, pendrin. Pendrin is stimulated by angiotensin II via the angiotensin type 1a receptor and by aldosterone through the mineralocorticoid receptor. Aldosterone stimulates pendrin expression and function, in part through the alkalosis it generates. Pendrin-mediated HCO3− secretion increases in models of metabolic alkalosis, which attenuates the alkalosis. However, pendrin positive ICs also regulate blood pressure, at least partly, through pendrin-mediated Cl− absorption, and through their indirect effect on the epithelial Na+ channel, ENaC. This aldosterone-induced increase in pendrin secondarily stimulates ENaC, thereby contributing to the aldosterone pressor response. This review describes the contribution of pendrin positive ICs to Na+, K+, Cl− and acid-base balance.