Inhibition of gastric motility by hyperglycemia is mediated by nodose ganglia KATP channels.

ABSTRACT: The inhibitory action of hyperglycemia is mediated by vagal afferent fibers innervating the stomach and duodenum. Our in vitro studies showed that a subset of nodose ganglia neurons is excited by rising ambient glucose, involving inactivation of ATP-sensitive K(+) (K(ATP)) channels and leading to membrane depolarization and neuronal firing. To investigate whether nodose ganglia K(ATP) channels mediate gastric relaxation induced by hyperglycemia, we performed in vivo gastric motility studies to examine the effects of K(ATP) channel activators and inactivators. Intravenous infusion of 20% dextrose induced gastric relaxation in a dose-dependent manner. This inhibitory effect of hyperglycemia was blocked by diazoxide, a K(ATP) channel activator. Conversely, tolbutamide, a K(ATP) channel inacti

SUBMITTER: Zhou SY 

PROVIDER: S-EPMC3064121 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature