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 alpha-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 alpha-adrenoceptor antagonists yohimbine (alpha(2)-adrenoceptor antagonist, 10(-8)-10(-6) M), prazosin (alpha(1)-adrenoceptor antagonist, 10(-9)-10(-7) M), 5-methyl-urapidil (5-MU, alpha(1A)-adrenoceptor antagonist, 10(-8)-10(-6) M), BMY 7378 (alpha(1D)-adrenoceptor antagonist, 10(-7)-10(-6) M), and chloroethylclonidine (CEC, irreversible alpha(1B)-adrenoceptor antagonist, 3x10(-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 (pA(2)-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 (pA(2)-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 alpha(2)-adrenoceptors, while in internal mammary artery it is mediated (to a major part) by alpha(1B)- and (to a minor part) by alpha(1A)-adrenoceptors.

AkrinorTM, a Cafedrine/ Theodrenaline Mixture (20:1), Increases Force of Contraction of Human Atrial Myocardium But Does Not Constrict Internal Mammary Artery In Vitro

“…Potency and E max of noradrenaline are in line with earlier reports on human IMA (EC 50 value of 560 vs. 660 nM) (Giessler et al, 2002). In contrast, Akrinor TM when applied alone was devoid of any vasoconstriction, suggesting absence of relevant α 1 -AR-agonistic activity.…”

Comparison of the Effects of Levosimendan and Papaverine on Human Internal Mammary Artery and Saphenous Vein

“…The different effects of levosimendan on human arterial and venous preparations may be due to the different pathways Values are means ± s. e. NE norepinephrine; IMA internal mammary artery; SV saphenous vein; NS, not significant of intracellular calcium increase and the role of the magnitude of K ATP channels in this process in these two vessels. It has been reported that the involved alphaadrenergic receptors in mediating NE-induced contraction in IMA and SV are different [13]. Based on the obtained results, levosimendan might be considered as a partial selective arteriodilator.…”

Topical Combinations to Treat Microvascular Dysfunction of Chronic Postischemia Pain

“…Regional blood flow is regulated by the vasoconstrictive transmitter norepinephrine (NE) released from sympathetic postganglionic neurons, which contracts vascular smooth muscles. 10,11 Blood flow is also regulated by the vasodilatory substance NO that is released from vascular endothelial cells and relaxes vascular smooth muscles. 12,13 Thus, drugs that reduce NE release or binding, or drugs that increase NO, can be used used to alleviate conditions with poor blood flow, 14,15 including microvascular dysfunction.…”