Lipopolysaccharides up-regulate Kir6.1/SUR2B channel expression and enhance vascular KATP channel activity via NF-kappaB-dependent signaling.

ABSTRACT: Sepsis is a severe medical condition causing a large number of deaths worldwide. Recent studies indicate that the septic susceptibility is attributable to the vascular ATP-sensitive K(+) (K(ATP)) channel. However, the mechanisms underlying the channel modulation in sepsis are still unclear. Here we show evidence for the modulation of vascular K(ATP) channel by septic pathogen lipopolysaccharides (LPS). In isolated mesenteric arterial rings, phenylephrine (PE) produced concentration-dependent vasoconstriction that was relaxed by pinacidil, a selective K(ATP) channel opener. The PE response was disrupted with a LPS treatment. In acutely dissociated aortic smooth myocytes the LPS treatment augmented K(ATP) channel activity, and hyperpolarized the cells. Quantitative PCR analysis showed that L

SUBMITTER: Shi W 

PROVIDER: S-EPMC2823456 | biostudies-literature | 2010 Jan

REPOSITORIES: biostudies-literature