Enhanced contribution of NO to exercise-induced coronary responses after alpha-adrenergic receptor blockade.
We hypothesized that nitric oxide (NO), in addition to beta-adrenergic effects, may contribute to exercise-induced coronary responses after alpha-adrenergic receptor blockade. Data were analyzed as relationships between coronary sinus (CS) O(2) saturation (CS O(2)sat) or coronary blood flow (CBF) and myocardial O(2) consumption (MVO(2)). As MVO(2) increased, CS O(2)sat fell more (P < 0.05) after N(omega)-nitro-L-arginine methyl ester (L-NAME; slope = -2.9 +/- 0.4 x 10(-2) %saturation. microl O(2) x min(-1) x g(-1)) than before (slope = -2.1 +/- 0.3 x 10(-2) %saturation. microl O(2). min(-1) x g(-1)). The slope of CBF versus MVO(2) was not altered. After blockade of alpha-adrenergic receptors alone (phentolamine), CS O(2)sat failed to decrease as MVO(2) increased (slope = -0.1 +/- 0.5 x 10(-2) %saturation. microl O(2) x min(-1) x g(-1)) x L-NAME given after phentolamine led to substantial decreases in CS O(2)sat (P < 0.01) as MVO(2) increased (slope = -2.1 +/- 0.4 x 10(-2) percent saturation. microl O(2)(-1) x min(-1) x g(-1)). CBF responses to exercise were smaller (P < 0.01) after phentolamine + L-NAME (slope = 6.1 +/- 0.1 x 10(-3) ml/microl O(2)) than after phentolamine alone (slope = 6.9 +/- 0.2 x 10(-3) ml/microl O(2)). Thus a significant portion of exercise-induced coronary responses after alpha-adrenergic receptor blockade involves NO formation.
Takamura
Masayuki
M
Department of Physiology, Faculty of Medicine, Université de Montréal, and Institut de Cardiologie de Montréal, Montréal, Québec, Canada H1T 1C8.
Parent
Robert
R
Lavallée
Michel
M
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D004285:Dogs; D004730:Endothelium, Vascular / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006339:Heart Rate / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D010101:Oxygen Consumption / Q000502:physiology; D010646:Phentolamine / Q000494:pharmacology*; D005082:Physical Exertion / Q000502:physiology*; D011433:Propranolol / Q000494:pharmacology; D017725:Ventricular Pressure / Q000502:physiology
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D011433:Propranolol; D019331:NG-Nitroarginine Methyl Ester; D010646:Phentolamine