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10.1172/jci.insight.92331 http://scihub22266oqcxt.onion/10.1172/jci.insight.92331 28931751!5621918!28931751     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight 2017 ; 2 (18): ä Nephropedia Template TP {{tp|p=28931751|t=2017. Essential role of Kir5 1 channels in renal salt handling and blood pressure control |pdf=|usr=}}{{28931751}} gab.com Text Essential role of Kir5 1 channels in renal salt handling and blood pressure control JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28931751 #FOAvip Supplementing diets with high potassium helps reduce hypertension in humans. Inwardly rectifying K+ channels Kir4.1 (Kcnj10) and Kir5.1 (Kcnj16) are highly expressed in the basolateral membrane of distal renal tubules and contribute to Na+ reabsorption and K+ secretion through the direct control of transepithelial voltage. To define the importance of Kir5.1 in blood pressure control under conditions of salt-induced hypertension, we generated a Kcnj16 knockout in Dahl salt-sensitive (SS) rats (SSKcnj16-/-). SSKcnj16-/- rats exhibited hypokalemia and reduced blood pressure, and when fed a high-salt diet (4% NaCl), experienced 100% mortality within a few days triggered by salt wasting and severe hypokalemia. Electrophysiological recordings of basolateral K+ channels in the collecting ducts isolated from SSKcnj16-/- rats revealed activity of only homomeric Kir4.1 channels. Kir4.1 expression was upregulated in SSKcnj16-/- rats, but the protein was predominantly localized in the cytosol in SSKcnj16-/- rats. Benzamil, but not hydrochlorothiazide or furosemide, rescued this phenotype from mortality on a high-salt diet. Supplementation of high-salt diet with increased potassium (2% KCl) prevented mortality in SSKcnj16-/- rats and prevented or mitigated hypertension in SSKcnj16-/- or control SS rats, respectively. Our results demonstrate that Kir5.1 channels are key regulators of renal salt handling in SS hypertension. Twit Text FOAVip Essential role of Kir5 1 channels in renal salt handling and blood pressure control ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28931751 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28931751 #FOAvip English Wikipedia <ref>{{Cite pmid|28931751}}</ref> Essential role of Kir5 1 channels in renal salt handling and blood pressure control #MMPMID28931751 Palygin O; Levchenko V; Ilatovskaya DV; Pavlov TS; Pochynyuk OM; Jacob HJ; Geurts AM; Hodges MR; Staruschenko A JCI Insight 2017[Sep]; 2 (18): ä PMID28931751show ga Supplementing diets with high potassium helps reduce hypertension in humans. Inwardly rectifying K+ channels Kir4.1 (Kcnj10) and Kir5.1 (Kcnj16) are highly expressed in the basolateral membrane of distal renal tubules and contribute to Na+ reabsorption and K+ secretion through the direct control of transepithelial voltage. To define the importance of Kir5.1 in blood pressure control under conditions of salt-induced hypertension, we generated a Kcnj16 knockout in Dahl salt-sensitive (SS) rats (SSKcnj16-/-). SSKcnj16-/- rats exhibited hypokalemia and reduced blood pressure, and when fed a high-salt diet (4% NaCl), experienced 100% mortality within a few days triggered by salt wasting and severe hypokalemia. Electrophysiological recordings of basolateral K+ channels in the collecting ducts isolated from SSKcnj16-/- rats revealed activity of only homomeric Kir4.1 channels. Kir4.1 expression was upregulated in SSKcnj16-/- rats, but the protein was predominantly localized in the cytosol in SSKcnj16-/- rats. Benzamil, but not hydrochlorothiazide or furosemide, rescued this phenotype from mortality on a high-salt diet. Supplementation of high-salt diet with increased potassium (2% KCl) prevented mortality in SSKcnj16-/- rats and prevented or mitigated hypertension in SSKcnj16-/- or control SS rats, respectively. Our results demonstrate that Kir5.1 channels are key regulators of renal salt handling in SS hypertension. |Amiloride/analogs & derivatives/pharmacology[MESH] |Animals[MESH] |Blood Pressure/*physiology[MESH] |Female[MESH] |Furosemide/pharmacology[MESH] |Hydrochlorothiazide/pharmacology[MESH] |Kidney Tubules, Distal/*metabolism[MESH] |Kir5.1 Channel[MESH] |Male[MESH] |Mutation[MESH] |Potassium Channels, Inwardly Rectifying/genetics/*physiology[MESH] |Rats[MESH] |Rats, Inbred Dahl[MESH] |Sodium Chloride, Dietary/administration & dosage[MESH]Essential role of Kir5 1 channels in renal salt handling and blood pre(epmc).pdf DeepDyve Pubget Overpricing