Vascular BK channel deficiency exacerbates organ damage and mortality in endotoxemic mice.

ABSTRACT: We determined the contribution of vascular BK channels to endotoxin (lipopolysaccharide, LPS)-induced hypotension, organ damage, and mortality using smooth muscle BK channel deficiency (BK channel β1-subunit knockout, BK β1-KO) mice. BK β1-KO mice were more sensitive to LPS-induced mortality compared with wild-type mice. After LPS (20 mg/kg, intraperitoneally), BK β1-KO mice had a more rapid fall in heart rate and blood pressure (measured by radiotelemetry), shorter latency to mortality, and higher mortality rate than wild-type mice. Twenty-two hours after LPS treatment, wild-type and BK β1-KO mice had reduced norepinephrine reactivity and impaired constrictor responses to the BK channel blocker paxilline in mesenteric arteries in vitro and higher iNOS expression in the heart, but not in m

SUBMITTER: Xu H 

PROVIDER: S-EPMC4327844 | biostudies-literature | 2012 Mar

REPOSITORIES: biostudies-literature