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ATP‐sensitive potassium channels mediate vasodilatation produced by calcitonin gene‐related peptide in human internal mammary but not gastroepiploic arteries
Author(s) -
LUU T. N.,
DASHWOOD M. R.,
TADJKARIMI S.,
CHESTER A. H.,
YACOUB M. H.
Publication year - 1997
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1997.2200764.x
Subject(s) - vasodilation , endocrinology , medicine , mammary artery , gastroepiploic artery , potassium channel , calcitonin , potassium , calcitonin gene related peptide , chemistry , neuropeptide , artery , receptor , bypass grafting , organic chemistry
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 μmol L −1 ) ( P < 0.05). In vitro autoradiography indicated that [ 125 I]‐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, K ATP channels are involved in the action of calcitonin gene‐related peptide in the internal mammary artery but not in the gastroepiploic artery.