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Am J Physiol Heart Circ Physiol 271: H1926-H1937, 1996;
0363-6135/96 $5.00
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AJP - Heart and Circulatory Physiology, Vol 271, Issue 5 1926-H1937, Copyright © 1996 by American Physiological Society

ARTICLES

Beta 2-adrenergic dilation of conductance coronary arteries involves flow-dependent NO formation in conscious dogs

N. Hamdad, Z. Ming, R. Parent and M. Lavallee
Department of Physiology, Faculty of Medicine, Universite de Montreal, Quebec, Canada.

The contribution of nitric oxide (NO) formation to the dilation of large epicardial coronary arteries to beta 1- and beta 2-adrenergic receptor stimulation was investigated in conscious dogs. After beta 1-adrenergic blockade (atenolol, 1.0 mg/kg iv), selective beta 2-adrenergic receptor activation with intracoronary bolus injections of pirbuterol (50 ng/kg) increased coronary blood flow (CBF) by 95 +/- 19% from 48.5 +/- 8.4 ml/min and external epicardial coronary diameter (CD) by 0.14 +/- 0.03 from 3.23 +/- 0.31 mm. After intracoronary N omega-nitro-L-arginine methyl ester (L-NAME, 50 micrograms.kg-1.min-1 x 12 min) was administered, baseline CD decreased but CBF was not altered. After L-NAME, bolus injections of pirbuterol resulted in smaller (P < 0.01) CBF responses (40 +/- 12%), and increases in CD were abolished. When pirbuterol (500 ng.kg-1.min-1) was given as a continuous infusion, CBF increased by 36 +/- 5% from 55.4 +/- 5.8 ml/min and CD by 0.16 +/- 0.03 mm from 3.44 +/- 0.16 mm. L-NAME abolished CD increases and limited (P < 0.01) CBF responses to 9 +/- 3%. When increases in CBF caused by pirbuterol before L-NAME were prevented by arterial constriction, CD increases were suppressed. In contrast, CBF and CD responses to beta 1-adrenergic stimulation were maintained after L-NAME. Thus beta 2-adrenergic dilation of epicardial conductance arteries is primarily a flow-dependent process involving NO formation. In contrast, beta 1-adrenergic activation produces epicardial coronary dilation independent of an L-NAME-sensitive mechanism.


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