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.
Department of Pharmacology, University of Wales College of Medicine, Heath Park, Cardiff.
H J
HJ
Taylor
A T
AT
Chaytor
W H
WH
Evans
T M
TM
Griffith
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001685:Biological Factors / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D017629:Gap Junctions / Q000187:drug effects*; D006034:Glycyrrhetinic Acid / Q000031:analogs & derivatives / Q000494:pharmacology*; D007083:Iliac Artery; D007211:Indoles / Q000494:pharmacology; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D011817:Rabbits; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology
D001685:Biological Factors; D007211:Indoles; D014665:Vasodilator Agents; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide; D000109:Acetylcholine; D006034:Glycyrrhetinic Acid; C000543:cyclopiazonic acid