Noradrenaline-induced contraction of human saphenous vein and human internal mammary artery: involvement of different α-adrenoceptor subtypes

Abstract.

Although saphenous veins and internal mammary arteries are commonly used for coronary artery bypass grafting, only a very few comparative studies are available on α-adrenoceptor-mediated vasoconstriction in these vessels. Thus, we determined, in isolated rings from human saphenous vein and human internal mammary artery, contractile responses to noradrenaline (10^–8–10^–4 M) in the absence and presence of the α-adrenoceptor antagonists yohimbine (α₂-adrenoceptor antagonist, 10^–8–10^–6 M), prazosin (α₁-adrenoceptor antagonist, 10^–9–10^–7 M), 5-methyl-urapidil (5-MU, α_1A-adrenoceptor antagonist, 10^–8–10^–6 M), BMY 7378 (α_1D-adrenoceptor antagonist, 10^–7–10^–6 M), and chloroethylclonidine (CEC, irreversible α_1B-adrenoceptor antagonist, 3×10^–5 M for 30 min). All experiments were carried out in the presence of 10^–7 M propranolol and 10^–5 M cocaine. In both vessel types noradrenaline evoked concentration-dependent contractions. In saphenous veins yohimbine was a potent antagonist (pA₂-value 8.32) while prazosin, 5-MU and BMY exhibited only marginal antagonistic effects. CEC, however, significantly decreased noradrenaline-induced contractions. In contrast, in internal mammary arteries prazosin (pA₂-value 9.65) and 5-MU (pK_B-values 7.2–7.5) were potent antagonists, while yohimbine and BMY exhibited only weak antagonistic effects. CEC, however, significantly decreased noradrenaline-induced contractions. We conclude that in saphenous vein the contractile response to noradrenaline is mediated predominantly by α₂-adrenoceptors, while in internal mammary artery it is mediated (to a major part) by α_1B- and (to a minor part) by α_1A-adrenoceptors.