Circulation, Vol 83, 2048-2056, Copyright © 1991 by American Heart Association
LR Pelc, GJ Gross and DC Warltier
BACKGROUND. Bradykinin has been demonstrated to be an endothelium-
dependent vasodilator in the cerebral circulation of the mouse, but the
actions of bradykinin on regional tissue perfusion in the canine coronary
circulation have not been studied. METHODS AND RESULTS. The mechanism of
coronary vasodilation by bradykinin was studied in open- chest,
anesthetized dogs. The role of cyclooxygenase stimulation, bradykinin B2
receptor activation, and endothelium-derived relaxing factor in
bradykinin-mediated vasodilation was studied in separate groups of dogs.
Bradykinin was infused intracoronarily so as to avoid changes in systemic
hemodynamics capable of altering the regional distribution of coronary
blood flow (radioactive microspheres). Bradykinin produced a preferential
increase in subendocardial blood flow. Pretreatment with indomethacin had
no effect on bradykinin- mediated increases in total left ventricular flow
or the transmural distribution of coronary blood flow. Blockade of
bradykinin B2 receptors with the competitive antagonist [Thi5,8,
D-Phe7]-bradykinin attenuated both the increase in total flow and
redistribution of perfusion to the subendocardium produced by bradykinin.
Inhibition of endothelium-derived relaxing factor with quinacrine,
occlusion/reperfusion, or NG-monomethyl L-arginine attenuated the total
increase in left ventricular flow and blocked the redistribution of flow to
the subendocardium produced by bradykinin. CONCLUSIONS. The present results
demonstrate that intracoronary infusion of bradykinin produces a
preferential increase in blood flow to the subendocardium via stimulation
of B2 receptors and the release of an endothelium- dependent relaxing
factor that may be nitric oxide.
ARTICLES
Mechanism of coronary vasodilation produced by bradykinin
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
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