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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刺激从孤立的小鼠连接肾小管和皮层收集管道插入的细胞中的H + -ATPase活性。

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Intercalated cells in the collecting duct system express V-type Hsup+/sup-ATPases which participate in acid extrusion, bicarbonate secretion, and chloride absorption depending on the specific subtype. The activity of Hsup+/sup-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 Hsup+/sup-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 Hsup+/sup-ATPase activity and localization in isolated mouse connecting tubules and cortical collecting ducts. Angiotensin II stimulated Nasup+/sup-independent intracellular pH recovery about 2-3 fold, and this was abolished by the specific Hsup+/sup-ATPase inhibitor concanamycin. The effect of angiotensin II was mediated through type 1 angiotensin II receptors (ATsub1/sub-receptors) because it could be blocked by saralasin. Stimulation of Hsup+/sup-ATPase activity required an intact microtubular network - it was completely inhibited by colchicine. Immunocytochemistry of isolated CNT/CCDs incubated iin vitro/i with angiotensin II suggests enhanced membrane associated staining of Hsup+/sup-ATPases in pendrin expressing intercalated cells. In summary, angiotensin II stimulates Hsup+/sup-ATPases in CNT/CCD intercalated cells, and may contribute to the regulation of chloride absorption and bicarbonate secretion in this nephron segment.
机译：收集管道系统中插入的细胞表达V型H + -ATPases，具体取决于特定的亚型，其参与酸挤出，碳酸氢盐分泌和氯离子吸收。 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，而H + -ATPases的活性激发了这一过程。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，我们研究了血管紧张素II（10 nM）对H + -ATPase活性和在分离的小鼠连接肾小管和皮层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，而特异性的H + -ATPase抑制剂伴刀豆球蛋白则取消了这一作用。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saralasin阻断。刺激H + -ATPase活性需要完整的微管网络-秋水仙碱完全抑制了它。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插层细胞中的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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