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Am J Physiol Heart Circ Physiol 282: H508-H515, 2002. First published October 11, 2001; doi:10.1152/ajpheart.00722.2001
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Vol. 282, Issue 2, H508-H515, February 2002

Enhanced contribution of NO to exercise-induced coronary responses after alpha -adrenergic receptor blockade

Masayuki Takamura, Robert Parent, and Michel Lavallée

Department of Physiology, Faculty of Medicine, Université de Montréal, and Institut de Cardiologie de Montréal, Montréal, Québec, Canada H1T 1C8

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) O2 saturation (CS O2sat) or coronary blood flow (CBF) and myocardial O2 consumption (MVO2). As MVO2 increased, CS O2sat fell more (P < 0.05) after Nomega -nitro-L-arginine methyl ester (L-NAME; slope = -2.9 ± 0.4 × 10-2 %saturation · µl O2 · min-1 · g-1) than before (slope = -2.1 ± 0.3 × 10-2 %saturation · µl O2 · min-1 · g-1). The slope of CBF versus MVO2 was not altered. After blockade of alpha -adrenergic receptors alone (phentolamine), CS O2sat failed to decrease as MVO2 increased (slope = -0.1 ± 0.5 × 10-2 %saturation · µl O2 · min-1 · g-1). L-NAME given after phentolamine led to substantial decreases in CS O2sat (P < 0.01) as MVO2 increased (slope = -2.1 ± 0.4 × 10-2 percent saturation · µl O2-1 · min-1 · g-1). CBF responses to exercise were smaller (P < 0.01) after phentolamine + L-NAME (slope = 6.1 ± 0.1 × 10-3 ml/µl O2) than after phentolamine alone (slope = 6.9 ± 0.2 × 10-3 ml/µl O2). Thus a significant portion of exercise-induced coronary responses after alpha -adrenergic receptor blockade involves NO formation.

endothelium; metabolism; oxygen; adrenergic receptors; coronary sinus


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