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10.1152/physiolgenomics.00122.2018 http://scihub22266oqcxt.onion/10.1152/physiolgenomics.00122.2018 30849009!6485378!30849009     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Physiol+Genomics 2019 ; 51 (4): 97-108 Nephropedia Template TP {{tp|p=30849009|t=2019. Genetic and genomic evidence for an important role of the Na(+)/H(+) exchanger 3 in blood pressure regulation and angiotensin II-induced hypertension |pdf=|usr=}}{{30849009}} gab.com Text Genetic and genomic evidence for an important role of the Na(+)/H(+) exchanger 3 in blood pressure regulation and angiotensin II-induced hypertension JO: Physiol Genomics http://www.kidney.de/pget.php?&tw=1&pmid=30849009 #FOAvip The sodium (Na(+))/hydrogen (H(+)) exchanger 3 (NHE3) and sodium-potassium adenosine triphosphatase (Na(+)/K(+)-ATPase) are two of the most important Na(+) transporters in the proximal tubules of the kidney. On the apical membrane side, NHE3 primarily mediates the entry of Na(+) into and the exit of H(+) from the proximal tubules, directly and indirectly being responsible for reabsorbing ~50% of filtered Na(+) in the proximal tubules of the kidney. On the basolateral membrane side, Na(+)/K(+)-ATPase serves as a powerful engine driving Na(+) out of, while pumping K(+) into the proximal tubules against their concentration gradients. While the roles of NHE3 and Na(+)/K(+)-ATPase in proximal tubular Na(+) transport under in vitro conditions are well recognized, their respective contributions to the basal blood pressure regulation and angiotensin II (ANG II)-induced hypertension remain poorly understood. Recently, we have been fortunate to be able to use genetically modified mouse models with global, kidney- or proximal tubule-specific deletion of NHE3 to directly determine the cause and effect relationship between NHE3, basal blood pressure homeostasis, and ANG II-induced hypertension at the whole body, kidney and/or proximal tubule levels. The purpose of this article is to review the genetic and genomic evidence for an important role of NHE3 with a focus in the regulation of basal blood pressure and ANG II-induced hypertension, as we learned from studies using global, kidney- or proximal tubule-specific NHE3 knockout mice. We hypothesize that NHE3 in the proximal tubules is necessary for maintaining basal blood pressure homeostasis and the development of ANG II-induced hypertension. Twit Text FOAVip Genetic and genomic evidence for an important role of the Na(+)/H(+) exchanger 3 in blood pressure regulation and angiotensin II-induced hypertension ????Physiol Genomics http://www.kidney.de/pget.php?&tw=1&pmid=30849009 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30849009 #FOAvip English Wikipedia <ref>{{Cite pmid|30849009}}</ref> Genetic and genomic evidence for an important role of the Na(+)/H(+) exchanger 3 in blood pressure regulation and angiotensin II-induced hypertension #MMPMID30849009 Li XC; Zheng X; Chen X; Zhao C; Zhu D; Zhang J; Zhuo JL Physiol Genomics 2019[Apr]; 51 (4): 97-108 PMID30849009show ga The sodium (Na(+))/hydrogen (H(+)) exchanger 3 (NHE3) and sodium-potassium adenosine triphosphatase (Na(+)/K(+)-ATPase) are two of the most important Na(+) transporters in the proximal tubules of the kidney. On the apical membrane side, NHE3 primarily mediates the entry of Na(+) into and the exit of H(+) from the proximal tubules, directly and indirectly being responsible for reabsorbing ~50% of filtered Na(+) in the proximal tubules of the kidney. On the basolateral membrane side, Na(+)/K(+)-ATPase serves as a powerful engine driving Na(+) out of, while pumping K(+) into the proximal tubules against their concentration gradients. While the roles of NHE3 and Na(+)/K(+)-ATPase in proximal tubular Na(+) transport under in vitro conditions are well recognized, their respective contributions to the basal blood pressure regulation and angiotensin II (ANG II)-induced hypertension remain poorly understood. Recently, we have been fortunate to be able to use genetically modified mouse models with global, kidney- or proximal tubule-specific deletion of NHE3 to directly determine the cause and effect relationship between NHE3, basal blood pressure homeostasis, and ANG II-induced hypertension at the whole body, kidney and/or proximal tubule levels. The purpose of this article is to review the genetic and genomic evidence for an important role of NHE3 with a focus in the regulation of basal blood pressure and ANG II-induced hypertension, as we learned from studies using global, kidney- or proximal tubule-specific NHE3 knockout mice. We hypothesize that NHE3 in the proximal tubules is necessary for maintaining basal blood pressure homeostasis and the development of ANG II-induced hypertension. |Angiotensin II/*pharmacology[MESH] |Animals[MESH] |Blood Pressure/*drug effects/*genetics[MESH] |Humans[MESH] |Hypertension/*chemically induced/*genetics[MESH] |Kidney Tubules, Proximal/drug effects[MESH]Genetic and genomic evidence for an important role of the Na(+)/H(+) e(epmc).pdf DeepDyve Pubget Overpricing