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10.1152/ajprenal.00292.2012 http://scihub22266oqcxt.onion/10.1152/ajprenal.00292.2012 C3680692!3680692 !23515718     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23515718 &cmd=llinks): Failed to open stream: HTTP request failed! 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Nitric oxide reduces Cl? absorption in the mouse cortical collecting duct through an ENaC-dependent mechanism |pdf=|usr=}}{{23515718 }} gab.com Text Nitric oxide reduces Cl absorption in the mouse cortical collecting duct through an ENaC-dependent mechanism JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=23515718 #FOAvip 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 ?M 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 ?M 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 ?M) 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?/HCO?? 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 ?M benzamil) to the perfusate. We conclude that NO reduces Cl? absorption in the CCD through a mechanism that is ENaC-dependent. Twit Text FOAVip Nitric oxide reduces Cl absorption in the mouse cortical collecting duct through an ENaC-dependent mechanism ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=23515718 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23515718 #FOAvip English Wikipedia <ref>{{Cite pmid|23515718 }}</ref> Nitric oxide reduces Cl? absorption in the mouse cortical collecting duct through an ENaC-dependent mechanism #MMPMID23515718 Pech V ; Thumova M ; Dikalov SI ; Hummler E ; Rossier BC ; Harrison DG ; Wall SM Am J Physiol Renal Physiol 2013[Jun]; 304 (11 ): F1390-7 PMID23515718 show ga 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 ?M 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 ?M 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 ?M) 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?/HCO?? 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 ?M benzamil) to the perfusate. We conclude that NO reduces Cl? absorption in the CCD through a mechanism that is ENaC-dependent. |Absorption/physiology [MESH] |Aldosterone/administration & dosage [MESH] |Amiloride/analogs & derivatives/pharmacology [MESH] |Angiotensin II/pharmacology [MESH] |Animals [MESH] |Anion Transport Proteins/deficiency/physiology [MESH] |Chloride-Bicarbonate Antiporters/physiology [MESH] |Chlorides/*metabolism [MESH] |Epithelial Sodium Channels/drug effects/genetics/*physiology [MESH] |Female [MESH] |In Vitro Techniques [MESH] |Kidney Tubules, Collecting/*metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Knockout [MESH] |NG-Nitroarginine Methyl Ester/pharmacology [MESH] |Nitric Oxide Donors/administration & dosage [MESH] |Nitric Oxide Synthase/antagonists & inhibitors [MESH] |Nitric Oxide/*physiology [MESH] |Sodium/pharmacology [MESH]Nitric oxide reduces Cl? absorption in the mouse cortical collecting d(epmc).pdf DeepDyve Pubget Overpricing