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Departments of 1 Medicine and 2 Physiology, Institut de Cardiologie de Montréal, Faculty of Medicine, Université de Montréal, Montréal, Québec, Canada H1T 1C8
We
hypothesized that endothelin (ET) release during exercise may be
triggered by 
-adrenergic-receptor activation and thereby influence
coronary hemodynamics and O2 metabolism in dogs. Exercise resulted in coronary blood flow increases (to 1.88 ± 0.26 from 1.10 ± 0.12 ml · min
1 · g1) and in a
fall (P < 0.01) in coronary sinus O2
saturation (17.4 ± 1.5 to 9.6 ± 0.7 vol%), whereas
myocardial O2 consumption
(M
O2) increased (109 ± 13% from
145 ± 16 µl
O2 · min1 · g1).
Tezosentan, a dual ETA/ETB-receptor blocker,
slightly reduced mean arterial pressure (MAP) and increased heart rate
throughout exercise. The relationship between coronary sinus
O2 saturation and MO2 was
shifted upward (P < 0.05) after tezosentan
administration; i.e., as MO2 increased
during exercise, coronary sinus O2 saturation was
disproportionately higher after ET-receptor blockade. After propranolol, tezosentan resulted in significant decreases
(P < 0.05) in left ventricular pressure, the first
derivative of left ventricular pressure over time, and MAP during
exercise. As MO2 increased during
exercise, coronary sinus O2 saturation levels after
tezosentan became superimposable over those observed before ET-receptor
blockade. Thus dual blockade of ETA/ETB
receptors alters coronary hemodynamics and O2 metabolism
during exercise, but ET activity failed to increase beyond baseline levels.
coronary blood flow; myocardial oxygen consumption; cardiac endothelin production
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