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-adrenergic receptor blockade
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
-adrenergic effects, may contribute to
exercise-induced coronary responses after
-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
(M
O2). As
M
O2 increased, CS O2sat fell
more (P < 0.05) after
N
-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 M
O2 was not
altered. After blockade of
-adrenergic receptors alone
(phentolamine), CS O2sat failed to decrease as
M
O2 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
M
O2 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
-adrenergic receptor
blockade involves NO formation.
endothelium; metabolism; oxygen; adrenergic receptors; coronary sinus
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