Key result
Pathophysiological levels of ET-1 impaired beta-adrenergic dilation of resistance coronary vessels through an ET(A) receptor-dependent process without impairing left ventricular inotropic responses.
Why the study?
Does pathophysiological plasma ET-1 impair beta-adrenergic dilation of coronary resistance vessels in conscious dogs?
Population
Conscious instrumented dogs
Comparison
Intravenous endothelin-1 infusion to reach… vs Baseline/control conditions without ET-1
Design
Preclinical
Authors
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Does not support clinical use of ETA antagonists for coronary dilation; extends preclinical evidence on ET-1 effects in conscious dogs.
Does pathophysiological plasma ET-1 impair beta-adrenergic dilation of coronary resistance vessels in conscious dogs?
Pathophysiological levels of ET-1 impair beta-adrenergic coronary dilation via an ETA receptor-dependent process, likely by interfering with smooth muscle KATP channels.
Okajima et al. (2004) studied this question. ET-1 intravenous infusions vs. Baseline/control conditions (dobutamine alone) was evaluated on Slopes of the Po(2)-MVo(2) and CBF-MVo(2) relations. Pathophysiological levels of ET-1 impaired beta-adrenergic dilation of resistance coronary vessels through an ET(A) receptor-dependent process without impairing left ventricular inotropic responses.
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