The gap junction inhibitor 18‐α‐glycyrrhetinic acid (α‐GA, 100 μM) attenuated endothelium‐dependent relaxations to acetylcholine and cyclopiazonic acid by ∼20% in rings of pre‐constricted rabbit iliac artery. The nitric oxide synthase inhibitor N^G‐nitro‐L‐arginine methyl ester (L‐NAME, 300 μM) inhibited relaxations to both agents by ∼65% and these were further attenuated by α‐GA to <10% of control. In endothelium‐denuded preparations, relaxations to sodium nitroprusside were not affected by α‐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.

British Journal of Pharmacology (1998) 125, 1–3; doi:10.1038/sj.bjp.0702078