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Articles in PresS, published online ahead of print October 11, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00722.2001
Submitted on August 13, 2001
Accepted on October 1, 2001
-adrenergic receptor blockade
1 Research Center, Montreal Heart Institute, Montreal, Quebec, Canada
2 Physiology, University of Montreal, Montreal, Quebec, Canada; Research Center, Montreal Heart Institute, Montreal, Quebec, Canada
* To whom correspondence should be addressed. E-mail: lavallem{at}icm.umontreal.ca.
We hypothesized that NO, in addition to ß-adrenergic effects, may contribute to exercise-induced coronary responses after -adrenergic receptor blockade.
Data were analysed as relationships between coronary sinus oxygen saturation (Cs O2 sat) or coronary blood flow (CBF) and MVO2. As MVO2 increased, Cs O2 sat fell more (P<.05) after N 
-nitro-L-arginine methyl ester (L-NAME, slope= -2.9±0.4 x 10-2%sat/µl O2.min-1.g-1.) than before (slope= -2.1±0.3 x 10-2 %sat/µl O2.min-1.g-1). The slope of CBF vs MVO2 was not altered. After blockade of -adrenergic receptors alone (phentolamine), Cs O2 sat failed to decrease as MVO2 increased (slope=-0.1± 0.5 x 10-2 %sat/µl O2.min-1.g-1). L-NAME given after phentolamine led to substantial decreases in Cs O2sat (P<.01) as MVO2 increased (slope= -2.1± 0.4 x 10-2%sat/µl O2.min-1.g-1.). CBF responses to exercise were smaller (P<.01) after phentolamine + L-NAME (slope= 6.1± 0.1 x 10-3.ml/µl O2) than after phentolamine alone (slope= 6.9± 0.2 x 10-3.ml/µl O2). Thus, a significant portion of exercise-induced coronary responses after -adrenergic receptor blockade involves NO formation.
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