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, α1A-adrenoceptor antagonist, 10–8–10–6 M), BMY 7378 (α1D-adrenoceptor antagonist, 10–7–10–6 M), and chloroethylclonidine (CEC, irreversible α1B-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 (pKB-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 α1B- and (to a minor part) by α1A-adrenoceptors.
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Giessler, C., Wangemann, T., Silber, RE. et al. Noradrenaline-induced contraction of human saphenous vein and human internal mammary artery: involvement of different α-adrenoceptor subtypes. Naunyn-Schmiedeberg's Arch Pharmacol 366, 104–109 (2002). https://doi.org/10.1007/s00210-002-0582-6
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DOI: https://doi.org/10.1007/s00210-002-0582-6