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- W2125967252 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 ( J Cl ) 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 J Cl and transepithelial voltage ( V T ) 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 J Cl 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 J Cl , we examined the effect of NO on J Cl 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 J Cl , NO modulates J Cl independent of the Na + -dependent Cl − /HCO 3 − exchanger (NDCBE, Slc4a8), the A cell apical plasma membrane H + -ATPase and pendrin. In contrast, both total and NO-sensitive J Cl and V T 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." @default.
- W2125967252 created "2016-06-24" @default.
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- W2125967252 date "2013-06-01" @default.
- W2125967252 modified "2023-10-16" @default.
- W2125967252 title "Nitric oxide reduces Cl<sup>−</sup>absorption in the mouse cortical collecting duct through an ENaC-dependent mechanism" @default.
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- W2125967252 doi "https://doi.org/10.1152/ajprenal.00292.2012" @default.
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