ArticleAmerican journal of physiology. Renal physiology2013
Nitric oxide reduces Cl⁻ absorption in the mouse cortical collecting duct through an ENaC-dependent mechanism.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed.
- Pendrin abundance, subcellular distribution, and function are unaffected by either αENaC gene ablation or by increasing ENaC channel activity.Pflugers Archiv : European journal of physiology · 2023Article
- 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
- The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.British journal of pharmacology · 2016Review
- The role of pendrin in blood pressure regulation.American journal of physiology. Renal physiology · 2016Review
- The chloride-bicarbonate exchanger pendrin is increased in the kidney of the pregnant rat.Experimental physiology · 2015Article
- ENaC inhibition stimulates HCl secretion in the mouse cortical collecting duct. II. Bafilomycin-sensitive H+ secretion.American journal of physiology. Renal physiology · 2015Article
- ENaC inhibition stimulates HCl secretion in the mouse cortical collecting duct. I. Stilbene-sensitive Cl- secretion.American journal of physiology. Renal physiology · 2015Article
- Renal NCC is unchanged in the midpregnant rat and decreased in the late pregnant rat despite avid renal Na+ retention.American journal of physiology. Renal physiology · 2015Article
- Impacts of nitric oxide and superoxide on renal medullary oxygen transport and urine concentration.American journal of physiology. Renal physiology · 2015Article
- Inhibition of ENaC by endothelin-1.Vitamins and hormones · 2015Review
- Regulatory roles of nitric oxide and angiotensin II on renal tubular transport.World journal of nephrology · 2014Review
- Function of cGMP-dependent protein kinase II in volume load-induced diuresis.Pflugers Archiv : European journal of physiology · 2014Article
- Cortical distal nephron Cl(-) transport in volume homeostasis and blood pressure regulation.American journal of physiology. Renal physiology · 2013Review
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7 authors.
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Abstract
Since nitric oxide (NO) participates in the renal regulation of blood pressure, in part, by modulating transport of Na⁺ and Cl⁻ in the kidney, we asked whether NO regulates net Cl⁻ flux (JCl) in the cortical collecting duct (CCD) and determined the transporter(s) that mediate NO-sensitive Cl⁻ absorption. Cl⁻ absorption was measured in CCDs perfused in vitro that were taken from aldosterone-treated mice. Administration of an NO donor (10 μM MAHMA NONOate) reduced JCl and transepithelial voltage (VT) both in the presence or absence of angiotensin II. However, reducing endogenous NO production by inhibiting NO synthase (100 μM N(G)-nitro-L-arginine methyl ester) increased JCl only in the presence of angiotensin II, suggesting that angiotensin II stimulates NO synthase activity. To determine the transport process that mediates NO-sensitive changes in JCl, we examined the effect of NO on JCl following either genetic ablation or chemical inhibition of transporters in the CCD. Since the application of hydrochlorothiazide (100 μM) or bafilomycin (5 nM) to the perfusate or ablation of the gene encoding pendrin did not alter NO-sensitive JCl, NO modulates JCl independent of the Na⁺-dependent Cl⁻/HCO₃⁻ exchanger (NDCBE, Slc4a8), the A cell apical plasma membrane H⁺-ATPase and pendrin. In contrast, both total and NO-sensitive JCl and VT were abolished with application of an epithelial Na(+) channel (ENaC) inhibitor (3 μM benzamil) to the perfusate. We conclude that NO reduces Cl⁻ absorption in the CCD through a mechanism that is ENaC-dependent.
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