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10.1681/ASN.2012080787 http://scihub22266oqcxt.onion/10.1681/ASN.2012080787 C3699825!3699825!23766534     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       J+Am+Soc+Nephrol 2013 ; 24 (7): 1104-13 Nephropedia Template TP {{tp|p=23766534|t=2013. Overexpression of Pendrin in Intercalated Cells Produces Chloride-Sensitive Hypertension |pdf=|usr=}}{{23766534}} gab.com Text Overexpression of Pendrin in Intercalated Cells Produces Chloride-Sensitive Hypertension JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=23766534 #FOAvip Inherited and acquired disorders that enhance the activity of transporters mediating renal tubular Na+ reabsorption are well established causes of hypertension. It is unclear, however, whether primary activation of an Na+-independent chloride transporter in the kidney can also play a pathogenic role in this disease. Here, mice overexpressing the chloride transporter pendrin in intercalated cells of the distal nephron (TgB1-hPDS mice) displayed increased renal absorption of chloride. Compared with normal mice, these transgenic mice exhibited a delayed increase in urinary NaCl and ultimately, developed hypertension when exposed to a high-salt diet. Administering the same sodium intake as NaHCO3 instead of NaCl did not significantly alter BP, indicating that the hypertension in the transgenic mice was chloride-sensitive. Moreover, excessive chloride absorption by pendrin drove parallel absorption of sodium through the epithelial sodium channel ENaC and the sodium-driven chloride/bicarbonate exchanger (Ndcbe), despite an appropriate downregulation of these sodium transporters in response to the expanded vascular volume and hypertension. In summary, chloride transport in the distal nephron can play a primary role in driving NaCl transport in this part of the kidney, and a primary abnormality in renal chloride transport can provoke arterial hypertension. Thus, we conclude that the chloride/bicarbonate exchanger pendrin plays a major role in controlling net NaCl absorption, thereby influencing BP under conditions of high salt intake. Twit Text FOAVip Overexpression of Pendrin in Intercalated Cells Produces Chloride-Sensitive Hypertension ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=23766534 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23766534 #FOAvip English Wikipedia <ref>{{Cite pmid|23766534}}</ref> Overexpression of Pendrin in Intercalated Cells Produces Chloride-Sensitive Hypertension #MMPMID23766534 Jacques T; Picard N; Miller RL; Riemondy KA; Houillier P; Sohet F; Ramakrishnan SK; Büsst CJ; Jayat M; Cornière N; Hassan H; Aronson PS; Hennings JC; Hübner CA; Nelson RD; Chambrey R; Eladari D J Am Soc Nephrol 2013[Jun]; 24 (7): 1104-13 PMID23766534show ga Inherited and acquired disorders that enhance the activity of transporters mediating renal tubular Na+ reabsorption are well established causes of hypertension. It is unclear, however, whether primary activation of an Na+-independent chloride transporter in the kidney can also play a pathogenic role in this disease. Here, mice overexpressing the chloride transporter pendrin in intercalated cells of the distal nephron (TgB1-hPDS mice) displayed increased renal absorption of chloride. Compared with normal mice, these transgenic mice exhibited a delayed increase in urinary NaCl and ultimately, developed hypertension when exposed to a high-salt diet. Administering the same sodium intake as NaHCO3 instead of NaCl did not significantly alter BP, indicating that the hypertension in the transgenic mice was chloride-sensitive. Moreover, excessive chloride absorption by pendrin drove parallel absorption of sodium through the epithelial sodium channel ENaC and the sodium-driven chloride/bicarbonate exchanger (Ndcbe), despite an appropriate downregulation of these sodium transporters in response to the expanded vascular volume and hypertension. In summary, chloride transport in the distal nephron can play a primary role in driving NaCl transport in this part of the kidney, and a primary abnormality in renal chloride transport can provoke arterial hypertension. Thus, we conclude that the chloride/bicarbonate exchanger pendrin plays a major role in controlling net NaCl absorption, thereby influencing BP under conditions of high salt intake. äOverexpression of Pendrin in Intercalated Cells Produces Chloride-Sens(epmc).pdf DeepDyve Pubget Overpricing