Key result
In isolated rat hearts, both BQ-123 and bosentan increased ET-1 efflux, but only BQ-123 exerted vasoconstrictor effects, suggesting ET-1 release is subject to negative feedback via ETA receptors.
Why the study?
Does ETA or ETA/ETB receptor antagonism affect coronary vasomotor tone, systolic function, and ET-1 efflux in isolated rat hearts with or without ischemia/reperfusion?
Population
Isolated rat hearts perfused using a Langendorff preparation (n=47)
Comparison
BQ-123 (10 M, ETA receptor antagonist) or… vs Control group (absence of ET antagonists)
Design
Preclinical
Follow-up
10 min pre-ischemia, 30 min ischemia, 30 min reperfusion
Authors
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ETA/ETB blockade effects on coronary tone need confirmation; leaves open optimal receptor targeting in humans.
Does ETA or ETA/ETB receptor antagonism affect coronary vasomotor tone, systolic function, and ET-1 efflux in isolated rat hearts with or without ischemia/reperfusion?
Selective ETA receptor antagonism with BQ-123 causes paradoxical vasoconstriction and increased ET-1 efflux in isolated rat hearts, likely via unopposed ETB stimulation.
Yi Zhang (1998) studied Myocardial ischemia/reperfusion (n=47). BQ-123 and bosentan vs. Control group (no ET antagonists) was evaluated on Coronary vasomotor tone, left ventricular systolic function and ET-1 efflux. In isolated rat hearts, both BQ-123 and bosentan increased ET-1 efflux, but only BQ-123 exerted vasoconstrictor effects, suggesting ET-1 release is subject to negative feedback via ETA receptors.
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