Salt-dependent inhibition of epithelial Na+ channel-mediated sodium reabsorption in the aldosterone-sensitive distal nephron by bradykinin.

ABSTRACT: We have documented recently that bradykinin (BK) directly inhibits activity of the epithelial Na(+) channel (ENaC) via the bradykinin B2 receptor (B2R)-G(q/11)-phospholipase C pathway. In this study, we took advantage of mice genetically engineered to lack bradykinin receptors (B1R, B2R(-/-)) to probe a physiological role of BK cascade in regulation of ENaC in native tissue, aldosterone-sensitive distal nephron. Under normal sodium intake (0.32% Na(+)), ENaC open probability (P(o)) was modestly elevated in B1R, B2R(-/-) mice compared with wild-type mice. This difference is augmented during elevated Na(+) intake (2.00% Na(+)) and negated during Na(+) restriction (<0.01% Na(+)). Saturation of systemic mineralocorticoid status with deoxycorticosterone acetate similarly increased ENaC activity

SUBMITTER: Mamenko M 

PROVIDER: S-EPMC3475746 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature