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10.1681/ASN.2013090936 http://scihub22266oqcxt.onion/10.1681/ASN.2013090936 C4073440!4073440!24480829     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2014 ; 25 (7): 1453-64 Nephropedia Template TP {{tp|p=24480829|t=2014. Colon-Specific Deletion of Epithelial Sodium Channel Causes Sodium Loss and Aldosterone Resistance |pdf=|usr=}}{{24480829}} gab.com Text Colon-Specific Deletion of Epithelial Sodium Channel Causes Sodium Loss and Aldosterone Resistance JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=24480829 #FOAvip Aldosterone promotes electrogenic sodium reabsorption through the amiloride-sensitive epithelial sodium channel (ENaC). Here, we investigated the importance of ENaC and its positive regulator channel-activating protease 1 (CAP1/Prss8) in colon. Mice lacking the ?ENaC subunit in colonic superficial cells (Scnn1aKO) were viable, without fetal or perinatal lethality. Control mice fed a regular or low-salt diet had a significantly higher amiloride-sensitive rectal potential difference (?PDamil) than control mice fed a high-salt diet. In Scnn1aKO mice, however, this salt restriction-induced increase in ?PDamil did not occur, and the circadian rhythm of ?PDamil was blunted. Plasma and urinary sodium and potassium did not change with regular or high-salt diets or potassium loading in control or Scnn1aKO mice. However, Scnn1aKO mice fed a low-salt diet lost significant amounts of sodium in their feces and exhibited high plasma aldosterone and increased urinary sodium retention. Mice lacking the CAP1/Prss8 in colonic superficial cells (Prss8KO) were viable, without fetal or perinatal lethality. Compared with controls, Prss8KO mice fed regular or low-salt diets exhibited significantly reduced ?PDamil in the afternoon, but the circadian rhythm was maintained. Prss8KO mice fed a low-salt diet also exhibited sodium loss through feces and higher plasma aldosterone levels. Thus, we identified CAP1/Prss8 as an in vivo regulator of ENaC in colon. We conclude that, under salt restriction, activation of the renin-angiotensin-aldosterone system in the kidney compensated for the absence of ENaC in colonic surface epithelium, leading to colon-specific pseudohypoaldosteronism type 1 with mineralocorticoid resistance without evidence of impaired potassium balance. Twit Text FOAVip Colon-Specific Deletion of Epithelial Sodium Channel Causes Sodium Loss and Aldosterone Resistance ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=24480829 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24480829 #FOAvip English Wikipedia <ref>{{Cite pmid|24480829}}</ref> Colon-Specific Deletion of Epithelial Sodium Channel Causes Sodium Loss and Aldosterone Resistance #MMPMID24480829 Malsure S; Wang Q; Charles RP; Sergi C; Perrier R; Christensen BM; Maillard M; Rossier BC; Hummler E J Am Soc Nephrol 2014[Jul]; 25 (7): 1453-64 PMID24480829show ga Aldosterone promotes electrogenic sodium reabsorption through the amiloride-sensitive epithelial sodium channel (ENaC). Here, we investigated the importance of ENaC and its positive regulator channel-activating protease 1 (CAP1/Prss8) in colon. Mice lacking the ?ENaC subunit in colonic superficial cells (Scnn1aKO) were viable, without fetal or perinatal lethality. Control mice fed a regular or low-salt diet had a significantly higher amiloride-sensitive rectal potential difference (?PDamil) than control mice fed a high-salt diet. In Scnn1aKO mice, however, this salt restriction-induced increase in ?PDamil did not occur, and the circadian rhythm of ?PDamil was blunted. Plasma and urinary sodium and potassium did not change with regular or high-salt diets or potassium loading in control or Scnn1aKO mice. However, Scnn1aKO mice fed a low-salt diet lost significant amounts of sodium in their feces and exhibited high plasma aldosterone and increased urinary sodium retention. Mice lacking the CAP1/Prss8 in colonic superficial cells (Prss8KO) were viable, without fetal or perinatal lethality. Compared with controls, Prss8KO mice fed regular or low-salt diets exhibited significantly reduced ?PDamil in the afternoon, but the circadian rhythm was maintained. Prss8KO mice fed a low-salt diet also exhibited sodium loss through feces and higher plasma aldosterone levels. Thus, we identified CAP1/Prss8 as an in vivo regulator of ENaC in colon. We conclude that, under salt restriction, activation of the renin-angiotensin-aldosterone system in the kidney compensated for the absence of ENaC in colonic surface epithelium, leading to colon-specific pseudohypoaldosteronism type 1 with mineralocorticoid resistance without evidence of impaired potassium balance. äColon-Specific Deletion of Epithelial Sodium Channel Causes Sodium Los(epmc).pdf DeepDyve Pubget Overpricing