Circulation, Vol 79, 1264-1270, Copyright © 1989 by American Heart Association
JS Weinstein, W Grossman, RM Weintraub, RL Thurer, RG Johnson and KG Morgan
Little 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.
ARTICLES
Differences in alpha-adrenergic responsiveness between human internal mammary arteries and saphenous veins
Charles A. Dana Research Institute, Beth Israel Hospital, Boston, MA 02215.
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