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Table of Contents
Vol. 35, No. 4, 1998
Issue release date: July – August
Section title: Research Paper
J Vasc Res 1998;35:285–294
(DOI:10.1159/000025595)

Characterization of Endothelium- Dependent Relaxation in Guinea Pig Basilar Artery – Effect of Hypoxia and Role of Cytochrome P450 Mono-Oxygenase

Petersson J. · Zygmunt P.M. · Jönsson P. · Högestätt E.D.
Department of Clinical Pharmacology, Institute of Laboratory Medicine, Lund University Hospital, Lund, Sweden

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Article / Publication Details

First-Page Preview
Abstract of Research Paper

Published online: August 07, 1998
Issue release date: July – August

Number of Print Pages: 10
Number of Figures: 0
Number of Tables: 0

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: http://www.karger.com/JVR

Abstract

In the guinea pig basilar artery, acetylcholine and the calcium ionophore A23187 induced endothelium-dependent relaxations, which were not significantly affected by the nitric oxide (NO) synthase inhibitor Nω-nitro-L-arginine (L-NOARG; 0.3 mM) or the guanylate cyclase inhibitor ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one; 1-10 µM), or by these inhibitors combined. However, acetylcholine (10 µM) and A23187 (3 µM) each significantly increased the tissue level of cGMP in the absence but not in the presence of L-NOARG, suggesting that NO is released from the vascular endothelium in this blood vessel. Treatment with the potassium (K) channel inhibitors charybdotoxin (0.1 µM) plus apamin (0.1 µM), a toxin mixture previously shown to inhibit relaxations mediated by endothelium-derived hyperpolarizing factor (EDHF) in this artery, had no effect on the A23187-induced relaxation but slightly inhibited the response to acetylcholine (Emax was reduced by 24%). When the action of EDHF was prevented by these K channel inhibitors, the remaining relaxation was abolished by either ODQ (1 µM) or L-NOARG (0.3 mM), indicating that NO, apart from EDHF, contributes to the endothelium-dependent relaxations. Furthermore, ODQ (10 µM) abolished the relaxation induced by the NO donor S-nitroso-N-acetylpenicillamine. Thus, activation of soluble guanylate cyclase seems to be the only mechanism through which NO causes relaxation in this artery. When vessels were exposed to grave hypoxia (pO2 = 6 mm Hg), the NO-mediated relaxation (induced by acetylcholine in the presence of charybdotoxin plus apamin) disappeared. In contrast, EDHF-mediated responses (elicited by acetylcholine in the presence of L-NOARG) were only marginally affected by hypoxia (Emax was reduced by 16%). 17-Octadecynoic acid (50 µM) and 5,8,11,14-eicosatetraynoic acid (10 µM), inhibitors of cytochrome P450-dependent oxidation of arachidonic acid, failed to inhibit the acetylcholine-induced relaxation in the presence of L-NOARG. The cytochrome P450-dependent arachidonic acid metabolite 11,12-epoxyecosatrienoic acid (0.3–3.0 µM) had no relaxant effect per se. In conclusion, EDHF and NO are both mediators of endothelium-dependent relaxations in the guinea pig basilar artery. However, during grave hypoxia, EDHF alone mediates acetylcholine-induced relaxation. The results further suggest that EDHF is not a metabolite of arachidonic acid formed by cytochrome P450 mono-oxygenase or generated by another oxygen-dependent enzyme in this artery.


Article / Publication Details

First-Page Preview
Abstract of Research Paper

Published online: August 07, 1998
Issue release date: July – August

Number of Print Pages: 10
Number of Figures: 0
Number of Tables: 0

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: http://www.karger.com/JVR


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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