Key result
ET(A) receptor blockade by darusentan prevented enhanced endothelium-dependent vasoconstriction to acetylcholine in obese mice lacking endothelial nitric oxide.
Why the study?
Does darusentan prevent enhanced endothelium-dependent vasoconstriction in obese mice during acute nitric oxide synthase inhibition?
Population
Obese C57Bl6/J mice fed on a high-fat diet for 30 weeks, and control mice
Comparison
ET receptor antagonist darusentan vs Untreated obese mice and control mice
Design
Preclinical
Authors
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ET(A) blockade may mitigate obesity-related endothelial dysfunction; leaves open clinical translation of darusentan.
Does darusentan prevent enhanced endothelium-dependent vasoconstriction in obese mice during acute nitric oxide synthase inhibition?
Endothelin modulates increased endothelium-dependent vasoconstriction in obesity, which can be prevented by chronic ET(A) receptor blockade.
Traupe et al. (2002) studied Obesity. Darusentan vs. Untreated obese mice and control mice was evaluated on Vascular reactivity in response to acetylcholine in the presence of acute inhibition of nitric oxide synthase. ET(A) receptor blockade by darusentan prevented enhanced endothelium-dependent vasoconstriction to acetylcholine in obese mice lacking endothelial nitric oxide.
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