Skip to main content
British Journal of Pharmacology logoLink to British Journal of Pharmacology
. 1998 Sep;125(1):1–3. doi: 10.1038/sj.bjp.0702078

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

Hannah J Taylor 2, Andrew T Chaytor 1, W Howard Evans 3, Tudor M Griffith 1,*
PMCID: PMC1565609  PMID: 9776336

Abstract

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 NG-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.

Keywords: Gap junctions, glycyrrhetinic acid, nitric oxide, endothelium-derived hyperpolarizing factor (EDHF)

Full Text

The Full Text of this article is available as a PDF (218.3 KB).


Articles from British Journal of Pharmacology are provided here courtesy of The British Pharmacological Society

RESOURCES