• J S Weinstein, W Grossman, R M Weintraub, R L Thurer, R G Johnson, and K G Morgan.
• Charles A. Dana Research Institute, Beth Israel Hospital, Boston, MA 02215.
• Circulation. 1989 Jun 1;79(6):1264-70.

AbstractLittle is known regarding specific biologic and pharmacologic differences between human internal mammary arteries and saphenous veins. To better define the role of alpha-adrenoceptor-mediated vasoconstriction in human internal mammary arteries and saphenous veins, we obtained fresh specimens of both vessels from 32 patients undergoing coronary artery bypass surgery. Dose-response curves were generated for the relatively selective alpha 1-receptor agonist phenylephrine, the alpha 2-receptor agonist BHT-920, and the alpha 1- and alpha 2-receptor agonist norepinephrine. Phenylephrine elicited similar contractile responses in internal mammary arteries and saphenous veins, with a mean EC50 (the effective concentration necessary to produce 50% of the maximal contraction) of 1.4 X 10(-6) M for internal mammary arteries and 1.8 X 10(-6) M for saphenous veins (p = NS). Selective stimulation of alpha 2-receptors with BHT-920 elicited a marked contractile response only in saphenous veins. Dose-response curves for phenylephrine and BHT-920 were shifted to the right for both vessels in the presence of the alpha 1-receptor antagonist prazosin and the alpha 2-receptor antagonist yohimbine, respectively. Norepinephrine elicited contraction at a lower concentration in saphenous veins than in internal mammary arteries with a mean EC50 of 7.8 X 10(-8) M for saphenous veins and a mean EC50 of 3.4 X 10(-7) M for internal mammary arteries (p less than 0.05). The results suggest that alpha-adrenoceptor-mediated vasoconstriction is caused primarily by alpha 1-receptors in human internal mammary arteries and by alpha 1- and alpha 2-receptors in human saphenous veins.

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