Inhibition of the gap junctional component of endothelium-dependent relaxations in rabbit iliac artery by 18-alpha glycyrrhetinic acid.

The gap junction inhibitor 18-alpha-glycyrrhetinic acid (alpha-GA, 100 microM) attenuated endothelium-dependent relaxations to acetylcholine and cyclopiazonic acid by approximately 20% in rings of pre-constricted rabbit iliac artery. The nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 300 microM) inhibited relaxations to both agents by approximately 65% and these were further attenuated by alpha-GA to < 10% of control. In endothelium-denuded preparations, relaxations to sodium nitroprusside were not affected by alpha-GA. Heterocellular gap junctional communication may therefore account for nitric oxide-independent relaxations evoked both by receptor-dependent and -independent mechanisms in rabbit iliac artery.