ATP‐sensitive potassium channels mediate vasodilatation produced by calcitonin gene‐related peptide in human internal mammary but not gastroepiploic arteries

Abstract

The purpose of this study was to elucidate the mechanism of action of calcitonin gene-related peptide-induced vasodilatation of human gastroepiploic and internal mammary arteries. Calcitonin gene-related peptide (0.1-100 nmol L-1) elicited relaxations of preconstricted vessels, with a significantly greater effect in the gastroepiploic artery (P < 0.05). This effect was independent of endothelium-derived vasodilating substances. The response of the internal mammary artery but not the gastroepiploic artery to calcitonin gene-related peptide was attenuated by glybenclamide (1.0 mumol L-1) (P < 0.05). In vitro autoradiography indicated that [125I]-calcitonin gene-related peptide bound to the tunica media but not the endothelial cells in both types of artery, with a significantly higher degree of binding in the gastroepiploic artery. It is concluded that calcitonin gene-related peptide acts directly on vascular smooth muscle via specific binding sites to induce vasodilatation. In addition, KATP channels are involved in the action of calcitonin gene-related peptide in the internal mammary artery but not in the gastroepiploic artery.

Comparison of vasodilators in human internal mammary artery: ghrelin is a potent physiological antagonist of endothelin‐1

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Sympathetic stimulation increases the blood flow through the in situ right gastroepiploic artery graft after off-pump coronary artery bypass graft surgery☆

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Release and effects of calcitonin gene-related peptide in myocardial ischaemia

“…These receptors are coupled to production of the second-messenger substance cyclic adenosine monophosphate (cAMP), and production of cAMP is regarded as the major mechanism for smooth muscle relaxation and vasodilation caused by CGRP (Edvinsson et al, 1985). However, additional mechanisms have been proposed to account for CGRP-induced vasodilation, including activation of K ATP channels (Nelson et al, 1990;Luu et al, 1997), and generation of NO (Gray and Marshall, 1992;Kim et al, 1995).…”