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Type: Journal article
Title: The effects of perhexiline on the rat coronary vasculature
Author: Kennedy, J.
Mohan, P.
Pelle, M.
Wade, S.
Horowitz, J.
Citation: European Journal of Pharmacology, 1999; 370(3):263-270
Issue Date: 1999
ISSN: 0014-2999
Statement of
Jennifer A. Kennedy, Puneet Mohan, Maria A. Pelle, Steven R. Wade, John D. Horowitz
Abstract: The predominant site and mechanism(s) of perhexiline-induced coronary vasodilatation were investigated in the rat heart. Perhexiline was more potent in the Langendorff perfused heart than in the left anterior descending coronary artery (EC50; 0.27 microM, confidence limits 0.19-0.39: 2.7 microM, 2.0-3.4, respectively). Selective endothelial inactivation with Triton X-100 in the perfused heart, reduced the response to perhexiline 1 microM (76+8% to 30+3% of control). 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) 3 microM, Nomega-nitro-L-arginine 100 microM, or a combination of the latter with indomethacin 10 microM, had no significant effect on responses to perhexiline in the perfused heart. Unlike bradykinin-induced vasodilatation, responses to perhexiline were not inhibited by tetrabutylammonium 1 mM, or charybdotoxin 20 nM. SKF525A 5 microM inhibited both perhexiline and bradykinin responses, while apamin 1 microM and glibenclamide 3 microM inhibited neither. Perhexiline exerts partially endothelium-dependent coronary vasodilator effects in the rat, predominantly on small coronary arteries, which appear to be independent of nitric oxide (NO), prostacyclin and the endothelium-derived hyperpolarising factor (EDHF) released by bradykinin.
Keywords: Muscle, Smooth
Coronary Vessels
Heart Ventricles
Nitric Oxide
Vasodilator Agents
Biological Factors
Dose-Response Relationship, Drug
Drug Interactions
In Vitro Techniques
DOI: 10.1016/S0014-2999(99)00106-5
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