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.