Open AccessEndothelium-Dependent Vasocontraction in Response to Noradrenaline in the Canine Cerebral Artery
Author(s) -
Hachiro Usui,
Kazuyoshi Kurahashi,
Hiroaki Shirahase,
Kiyoshi Fukui,
Motohatsu Fujiwara
Publication year - 1987
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.44.228
Subject(s) - yohimbine , contraction (grammar) , endothelium , cerebral arteries , basilar artery , prazosin , medicine , vasoconstriction , endocrinology , cardiology , anatomy , antagonist , receptor
In the canine basilar artery, noradrenaline-induced contraction was markedly decreased by intimal rubbing. Scanning electron microscopic studies showed that the rubbing procedure had scrapped away the endothelial cells from the intimal surface of the artery. Prazosin (10(-7) M) reduced the noradrenaline-induced contraction in intact arteries, but did not significantly affect the contraction in the scrapped arteries. Yohimbine (10(-7) M) strongly inhibited the contraction in both intact and scrapped arteries. The endothelium-dependent vasocontraction produced by noradrenaline was inhibited by aspirin (5 X 10(-5) M), OKY-046 (10(-5) M) and ONO-3708 (5 X 10(-9) M). The present experiments provided evidence for endothelium-dependence of the vasocontraction produced by noradrenaline in canine basilar arteries, and they suggested that the endothelium-derived contracting factors might be arachidonic acid metabolites such as TXA2; they also suggested that alpha 1 adrenoceptors might be preferentially distributed on the endothelium, while alpha 2 adrenoceptors are preferentially located in smooth muscle.