The effect of glucagon on vasoconstriction and vascular escape from nerve- and norepinephrine-induced constriction of the hepatic artery of the cat

Abstract

Glucagon, in the anesthetized cat, was capable of dilating the hepatic artery to the same extent and in a dose-dependent manner when administered directly into the hepatic artery or into the portal vein. Portal venous infusions of glucagon did not inhibit nerve- or norepinephrine-induced vasoconstriction of the hepatic artery in contrast to previous reports in the dog. Rather, at certain doses, glucagon mildly potentiated the vasoconstriction induced by both constrictor stimuli. Vascular escape from nerve- and norepinephrine-induced constrictor responses was found to be inhibited by glucagon in a dose-dependent manner. Glucagon infusion is the first intervention reported to modulate vascular escape in the hepatic artery. Owing to its similar effects on nerve- and exogenous norepinephrine-induced responses, glucagon appears to be acting at a postsynaptic site. Therefore, we suggest that in the cat, glucagon is not an inhibitory modulator of nerve- and norepinephrine-induced vasoconstriction, but rather may potentiate the constrictor response in a postsynaptic manner.Key words: glucagon, hepatic artery, modulation, vascular escape, vasoconstriction.