Beta2-adrenergic dilation of conductance coronary arteries involves
flow-dependent no formation in conscious dogs.
Hamdad, Nadia, Zhi Ming, Robert Parent, and Michel Lavall[acute]ee.
Department of Physiology, Faculty of Medicine, Universit[acute]e de
Montr[acute]eal and Institut de Cardiologie de Montr[acute]eal,
Montr[acute]eal, Qu[acute]ebec, Canada
APStracts 3:0203H, 1996.
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 (ic) 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 ic
N_-nitro-L-arginine methyl ester (L-NAME, 50 [mu]g/kg/min x 12 min),
baseline CD fell but CBF was not altered. After L-NAME, bolus
injections of pirbuterol resulted in smaller (P<.01) CBF
responses (40+/-12 %) and increases in CD were abolished. Given as a
continuous infusion, pirbuterol (500 ng/kg/min) increased CBF by
36+/-5 % from 55.4+/-5.8 mL/min and CD by 0.16+/-0.03 from 3.44+/
-0.16 mm. L-NAME abolished CD increases and limited (P<.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.
Received 7 February 1996; accepted in final form 15 April 1996.
APS Manuscript Number H119-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 May 96