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首页> 外文期刊>Cellular Physiology and Biochemistry >Angiotensin II stimulates H-ATPase activity in intercalated cells from isolated mouse connecting tubules and cortical collecting ducts
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Angiotensin II stimulates H-ATPase activity in intercalated cells from isolated mouse connecting tubules and cortical collecting ducts

机译：血管紧张素II刺激分离的小鼠连接肾小管和皮层收集管的插层细胞中的H-ATPase活性

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摘要

Intercalated cells in the collecting duct system express V-type H ~+-ATPases which participate in acid extrusion, bicarbonate secretion, and chloride absorption depending on the specific subtype. The activity of H~+-ATPases is regulated by acid-base status and several hormones, including angiotensin II and aldosterone. Angiotensin II stimulates chloride absorption mediated by pendrin in type B intercalated cells and this process is energized by the activity of H~+-ATPases. Moreover, angiotensin II stimulates bicarbonate secretion by the connecting tubule (CNT) and early cortical collecting duct (CCD). In the present study we examined the effect of angiotensin II (10 nM) on H~+-ATPase activity and localization in isolated mouse connecting tubules and cortical collecting ducts. Angiotensin II stimulated Na~+-independent intracellular pH recovery about 2-3 fold, and this was abolished by the specific H~+-ATPase inhibitor concanamycin. The effect of angiotensin II was mediated through type 1 angiotensin II receptors (AT_1-receptors) because it could be blocked by saralasin. Stimulation of H~+-ATPase activity required an intact microtubular network-it was completely inhibited by colchicine. Immunocytochemistry of isolated CNT/CCDs incubated in vitro with angiotensin II suggests enhanced membrane associated staining of H~+-ATPases in pendrin expressing intercalated cells. In summary, angiotensin II stimulates H~+-ATPases in CNT/CCD intercalated cells, and may contribute to the regulation of chloride absorption and bicarbonate secretion in this nephron segment.
机译：收集管道系统中的插层细胞表达V型H〜+ -ATPases，这些酶参与酸的挤出，碳酸氢盐的分泌和氯离子的吸收，具体取决于特定的亚型。 H〜+ -ATPases的活性受酸碱状态和几种激素（包括血管紧张素II和醛固酮）的调节。血管紧张素II刺激了Pendrin在B型插层细胞中介导的氯化物吸收，并且该过程由H〜+ -ATPase的活性激发。此外，血管紧张素II通过连接小管（CNT）和早期皮质收集管（CCD）刺激碳酸氢盐分泌。在本研究中，我们检查了血管紧张素II（10 nM）对H〜+ -ATPase活性和在孤立的小鼠连接肾小管和皮质收集管中的定位的影响。血管紧张素II刺激不依赖Na〜+的细胞内pH恢复约2-3倍，并且被特异性的H〜+ -ATPase抑制剂伴刀豆球蛋白所取消。血管紧张素II的作用是通过1型血管紧张素II受体（AT_1-受体）介导的，因为它可以被萨拉信素阻断。刺激H〜+ -ATPase活性需要完整的微管网络-秋水仙碱可完全抑制它。体外与血管紧张素II孵育的分离的CNT / CCD的免疫细胞化学表明，表达Pendrin的插层细胞中H〜+ -ATPase的膜相关染色增强。总之，血管紧张素II刺激CNT / CCD插入细胞中的H〜+ -ATPase，并可能有助于调节该肾单位节段中氯的吸收和碳酸氢盐的分泌。

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