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10.14814/phy2.15080 http://scihub22266oqcxt.onion/10.14814/phy2.15080 34665521!8525323!34665521     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Physiol+Rep 2021 ; 9 (20): e15080 Nephropedia Template TP {{tp|p=34665521|t=2021. Role of collecting duct principal cell NOS1beta in sodium and potassium homeostasis |pdf=|usr=}}{{34665521}} gab.com Text Role of collecting duct principal cell NOS1beta in sodium and potassium homeostasis JO: Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=34665521 #FOAvip The nitric oxide (NO)-generating enzyme, NO synthase-1beta (NOS1beta), is essential for sodium (Na(+) ) homeostasis and blood pressure control. We previously showed that collecting duct principal cell NOS1beta is critical for inhibition of the epithelial sodium channel (ENaC) during high Na(+) intake. Previous studies on freshly isolated cortical collecting ducts (CCD) demonstrated that exogenous NO promotes basolateral potassium (K(+) ) conductance through basolateral channels, presumably K(ir) 4.1 (Kcnj10) and K(ir) 5.1 (Kcnj16). We, therefore, investigated the effects of NOS1beta knockout on K(ir) 4.1/K(ir) 5.1 channel activity. Indeed, in CHO cells overexpressing NOS1beta and K(ir) 4.1/K(ir) 5.1, the inhibition of NO signaling decreased channel activity. Male littermate control and principal cell NOS1beta knockout mice (CDNOS1KO) on a 7-day, 4% NaCl diet (HSD) were used to detect changes in basolateral K(+) conductance. We previously demonstrated that CDNOS1KO mice have high circulating aldosterone despite a high-salt diet and appropriately suppressed renin. We observed greater K(ir) 4.1 cortical abundance and significantly greater K(ir) 4.1/K(ir) 5.1 single-channel activity in the principal cells from CDNOS1KO mice. Moreover, blocking aldosterone action with in vivo spironolactone treatment resulted in lower K(ir) 4.1 abundance and greater plasma K(+) in the CDNOS1KO mice compared to controls. Lowering K(+) content in the HSD prevented the high aldosterone and greater plasma Na(+) of CDNOS1KO mice and normalized K(ir) 4.1 abundance. We conclude that during chronic HSD, lack of NOS1beta leads to increased plasma K(+) , enhanced circulating aldosterone, and activation of ENaC and K(ir) 4.1/K(ir) 5.1 channels. Thus, principal cell NOS1beta is required for the regulation of both Na(+) and K(+) by the kidney. Twit Text FOAVip Role of collecting duct principal cell NOS1beta in sodium and potassium homeostasis ????Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=34665521 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34665521 #FOAvip English Wikipedia <ref>{{Cite pmid|34665521}}</ref> Role of collecting duct principal cell NOS1beta in sodium and potassium homeostasis #MMPMID34665521 Hyndman KA; Isaeva E; Palygin O; Mendoza LD; Rodan AR; Staruschenko A; Pollock JS Physiol Rep 2021[Oct]; 9 (20): e15080 PMID34665521show ga The nitric oxide (NO)-generating enzyme, NO synthase-1beta (NOS1beta), is essential for sodium (Na(+) ) homeostasis and blood pressure control. We previously showed that collecting duct principal cell NOS1beta is critical for inhibition of the epithelial sodium channel (ENaC) during high Na(+) intake. Previous studies on freshly isolated cortical collecting ducts (CCD) demonstrated that exogenous NO promotes basolateral potassium (K(+) ) conductance through basolateral channels, presumably K(ir) 4.1 (Kcnj10) and K(ir) 5.1 (Kcnj16). We, therefore, investigated the effects of NOS1beta knockout on K(ir) 4.1/K(ir) 5.1 channel activity. Indeed, in CHO cells overexpressing NOS1beta and K(ir) 4.1/K(ir) 5.1, the inhibition of NO signaling decreased channel activity. Male littermate control and principal cell NOS1beta knockout mice (CDNOS1KO) on a 7-day, 4% NaCl diet (HSD) were used to detect changes in basolateral K(+) conductance. We previously demonstrated that CDNOS1KO mice have high circulating aldosterone despite a high-salt diet and appropriately suppressed renin. We observed greater K(ir) 4.1 cortical abundance and significantly greater K(ir) 4.1/K(ir) 5.1 single-channel activity in the principal cells from CDNOS1KO mice. Moreover, blocking aldosterone action with in vivo spironolactone treatment resulted in lower K(ir) 4.1 abundance and greater plasma K(+) in the CDNOS1KO mice compared to controls. Lowering K(+) content in the HSD prevented the high aldosterone and greater plasma Na(+) of CDNOS1KO mice and normalized K(ir) 4.1 abundance. We conclude that during chronic HSD, lack of NOS1beta leads to increased plasma K(+) , enhanced circulating aldosterone, and activation of ENaC and K(ir) 4.1/K(ir) 5.1 channels. Thus, principal cell NOS1beta is required for the regulation of both Na(+) and K(+) by the kidney. |*Homeostasis[MESH] |Animals[MESH] |CHO Cells[MESH] |Cricetinae[MESH] |Cricetulus[MESH] |Ion Transport[MESH] |Kidney Tubules, Collecting/*metabolism[MESH] |Male[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Nitric Oxide Synthase Type I/*physiology[MESH] |Potassium Channels, Inwardly Rectifying/genetics/*metabolism[MESH] |Potassium/*metabolism[MESH]Role of collecting duct principal cell NOS1beta in sodium and potassiu(epmc).pdf DeepDyve Pubget Overpricing