Mineralocorticoid receptor-independent activation of ENaC in bile duct ligated mice.

ABSTRACT: Sodium and fluid retention in liver disease is classically thought to result from reduced effective circulating volume and stimulation of the renin-angiotensin-aldosterone system (RAAS). Aldosterone dives Na⁺ retention by activating the mineralocorticoid receptor and promoting the maturation and apical surface expression of the epithelial Na⁺ channel (ENaC), found in the aldosterone-sensitive distal nephron. However, evidence of fluid retention without RAAS activation suggests the involvement of additional mechanisms. Liver disease can greatly increase plasma and urinary bile acid concentrations and have been shown to activate ENaC in vitro. We hypothesize that elevated bile acids in liver disease activate ENaC and drive fluid retention independent of RAAS. We

SUBMITTER: Wang XP 

PROVIDER: S-EPMC10542149 | biostudies-literature | 2023 Sep

REPOSITORIES: biostudies-literature