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Inhibition of the gap junctional component of endothelium‐dependent relaxations in rabbit iliac artery by 18‐ α glycyrrhetinic acid
Author(s) -
Taylor Hannah J,
Chaytor Andrew T,
Evans W Howard,
Griffith Tudor M
Publication year - 1998
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0702078
Subject(s) - cyclopiazonic acid , sodium nitroprusside , nitric oxide , endothelium , gap junction , nitric oxide synthase , acetylcholine , chemistry , pharmacology , biophysics , biochemistry , biology , endocrinology , endoplasmic reticulum , intracellular
The gap junction inhibitor 18‐α‐glycyrrhetinic acid (α‐GA, 100 μ M ) 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 μ M ) 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