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10.1038/pr.2014.145 http://scihub22266oqcxt.onion/10.1038/pr.2014.145 C4268054!4268054!25279988     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Pediatr+Res 2015 ; 77 (ä): 64-9 Nephropedia Template TP {{tp|p=25279988|t=2015. Impaired epithelial Na+ channels activity contributes to cystogenesis and development of autosomal recessive polycystic kidney disease in PCK rats |pdf=|usr=}}{{25279988}} gab.com Text Impaired epithelial Na+ channels activity contributes to cystogenesis and development of autosomal recessive polycystic kidney disease in PCK rats JO: Pediatr Res http://www.kidney.de/pget.php?&tw=1&pmid=25279988 #FOAvip BACKGROUND: Autosomal recessive polycystic kidney disease (ARPKD) is a genetic disorder characterized by the development of renal cysts of the tubular epithelial cell origin. Epithelial Na+ channel (ENaC) is responsible for sodium reabsorption in the aldosterone-sensitive distal nephron. Here we investigated the ENaC expression and activity in cystic tissue taken from rats with ARPKD. METHODS: PCK rats were treated with the selective ENaC inhibitor benzamil given in the drinking water, and after 4 or 12 weeks the severity of morphological malformations in the kidneys was assessed. ENaC and AQP2 expression and ENaC activity were tested with immunohistochemistry and patch clamp electrophysiology, respectively. RESULTS: Treatment with benzamil exacerbated development of cysts compared to the vehicle-treated animals. In contrast, the 12 weeks treatment with a loop diuretic furosemide had no effect on cystogenesis. Single channel patch clamp analysis revealed that ENaC activity in the freshly isolated cystic epithelium was significantly lower than in the non-cystic collecting ducts isolated from PCK or normal Sprague-Dawley rats. Immunohistochemical analysis confirmed that ?-ENaC and AQP2 expressions in cysts are decreased compared to non-dilated tubules from PCK rat kidneys. CONCLUSION: We demonstrated that cystic epithelium exhibits low ENaC activity and this phenomenon can contribute to cyst progression. Twit Text FOAVip Impaired epithelial Na+ channels activity contributes to cystogenesis and development of autosomal recessive polycystic kidney disease in PCK rats ????Pediatr Res http://www.kidney.de/pget.php?&tw=1&pmid=25279988 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25279988 #FOAvip English Wikipedia <ref>{{Cite pmid|25279988}}</ref> Impaired epithelial Na+ channels activity contributes to cystogenesis and development of autosomal recessive polycystic kidney disease in PCK rats #MMPMID25279988 Pavlov TS; Levchenko V; Ilatovskaya DV; Palygin O; Staruschenko A Pediatr Res 2015[Jan]; 77 (ä): 64-9 PMID25279988show ga BACKGROUND: Autosomal recessive polycystic kidney disease (ARPKD) is a genetic disorder characterized by the development of renal cysts of the tubular epithelial cell origin. Epithelial Na+ channel (ENaC) is responsible for sodium reabsorption in the aldosterone-sensitive distal nephron. Here we investigated the ENaC expression and activity in cystic tissue taken from rats with ARPKD. METHODS: PCK rats were treated with the selective ENaC inhibitor benzamil given in the drinking water, and after 4 or 12 weeks the severity of morphological malformations in the kidneys was assessed. ENaC and AQP2 expression and ENaC activity were tested with immunohistochemistry and patch clamp electrophysiology, respectively. RESULTS: Treatment with benzamil exacerbated development of cysts compared to the vehicle-treated animals. In contrast, the 12 weeks treatment with a loop diuretic furosemide had no effect on cystogenesis. Single channel patch clamp analysis revealed that ENaC activity in the freshly isolated cystic epithelium was significantly lower than in the non-cystic collecting ducts isolated from PCK or normal Sprague-Dawley rats. Immunohistochemical analysis confirmed that ?-ENaC and AQP2 expressions in cysts are decreased compared to non-dilated tubules from PCK rat kidneys. CONCLUSION: We demonstrated that cystic epithelium exhibits low ENaC activity and this phenomenon can contribute to cyst progression. äImpaired epithelial Na+ channels activity contributes to cystogenesis (epmc).pdf DeepDyve Pubget Overpricing