ArticleAmerican journal of physiology. Renal physiology2015
ENaC inhibition stimulates HCl secretion in the mouse cortical collecting duct. I. Stilbene-sensitive Cl- secretion.
Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Pendrin: linking acid base to blood pressure.Pflugers Archiv : European journal of physiology · 2024Review
- Regulation of Blood Pressure and Salt Balance By Pendrin-Positive Intercalated Cells: Donald Seldin Lecture 2020.Hypertension (Dallas, Tex. : 1979) · 2022Review
- The Renal Physiology of Pendrin-Positive Intercalated Cells.Physiological reviews · 2020Review
- α-Ketoglutarate stimulates pendrin-dependent ClAmerican journal of physiology. Renal physiology · 2018Article
- The Role of Intercalated CellJournal of the American Society of Nephrology : JASN · 2018Article
- Barttin Regulates the Subcellular Localization and Posttranslational Modification of Human ClFrontiers in physiology · 2018Article
- Renal intercalated cells and blood pressure regulation.Kidney research and clinical practice · 2017Review
- The role of pendrin in blood pressure regulation.American journal of physiology. Renal physiology · 2016Review
- Chloride secretion by renal collecting ducts.Current opinion in nephrology and hypertension · 2015Article
- ENaC inhibition stimulates HCl secretion in the mouse cortical collecting duct. II. Bafilomycin-sensitive H+ secretion.American journal of physiology. Renal physiology · 2015Article
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9 authors.
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Abstract
Inhibition of the epithelial Na(+) channel (ENaC) reduces Cl(-) absorption in cortical collecting ducts (CCDs) from aldosterone-treated rats and mice. Since ENaC does not transport Cl(-), the purpose of the present study was to explore how ENaC modulates Cl(-) absorption in mouse CCDs perfused in vitro. Therefore, we measured transepithelial Cl(-) flux and transepithelial voltage in CCDs perfused in vitro taken from mice that consumed a NaCl-replete diet alone or the diet with aldosterone administered by minipump. We observed that application of an ENaC inhibitor [benzamil (3 μM)] to the luminal fluid unmasks conductive Cl(-) secretion. During ENaC blockade, this Cl(-) secretion fell with the application of a nonselective Cl(-) channel blocker [DIDS (100 μM)] to the perfusate. While single channel recordings of intercalated cell apical membranes in split-open CCDs demonstrated a Cl(-) channel with properties that resemble the ClC family of Cl(-) channels, ClC-5 is not the primary pathway for benzamil-sensitive Cl(-) flux. In conclusion, first, in CCDs from aldosterone-treated mice, most Cl(-) absorption is benzamil sensitive, and, second, benzamil application stimulates stilbene-sensitive conductive Cl(-) secretion, which occurs through a ClC-5-independent pathway.
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