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

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  • 1. Department of Pharmacology, University of Wales College of Medicine, Heath Park, Cardiff.
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    • Taylor HJ 1
    (1 author)

British Journal of Pharmacology, 01 Sep 1998, 125(1):1-3
https://doi.org/10.1038/sj.bjp.0702078 PMID: 9776336 PMCID: PMC1565609

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Abstract 

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.

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Br J Pharmacol. 1998 Sep; 125(1): 1–3.
PMCID: PMC1565609
PMID: 9776336

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 and Tudor M Griffith1,*
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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)

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