Key result
Endothelin-1 regulates coronary circulation via ETA-mediated constriction and ETB-mediated dilation, suggesting ET receptor blockade may improve the match between metabolic demand and perfusion.
Why the study?
Does ET receptor blockade improve the match between cardiac metabolic demand and coronary perfusion in the context of elevated ET-1 levels?
Population
Coronary vessels (human and canine models) in healthy states and heart failure
Design
Review
Authors
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ET-1 coronary effects may support ETA-targeted exploration in HF; leaves open clinical efficacy pending prospective trials.
Does ET receptor blockade improve the match between cardiac metabolic demand and coronary perfusion in the context of elevated ET-1 levels?
This review highlights the role of ET-1 in coronary vasoconstriction via ETA receptors and suggests ET receptor blockade as a potential mechanism to improve coronary perfusion in conditions like heart failure.
Lavallée et al. (2003) conducted a review in Heart failure. Endothelin-1 (ET-1) was evaluated. Endothelin-1 regulates coronary circulation via ETA-mediated constriction and ETB-mediated dilation, suggesting ET receptor blockade may improve the match between metabolic demand and perfusion.
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