Key result
Carotid artery relaxation in response to acetylcholine was impaired in eNOS-deficient mice (55% in +/- and 0% in -/- vs 83% in wild-type, P<0.001), while relaxation to nitroprusside was enhanced.
Why the study?
Does eNOS deficiency alter vascular relaxation responses to acetylcholine and nitroprusside in mouse carotid arteries?
Population
Carotid arteries from heterozygous and homozygous endothelial nitric oxide synthase-deficient mice and…
Comparison
In vitro administration of acetylcholine and… vs Responses in wild-type eNOS(+/+) littermates
Design
Preclinical
Authors
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eNOS deficiency impairs endothelium-dependent relaxation in mice; leaves open relevance to human endothelial dysfunction or NO donor therapy.
Does eNOS deficiency alter vascular relaxation responses to acetylcholine and nitroprusside in mouse carotid arteries?
Absolute Event Rate: 0% vs 83%
p-value: p=<0.001
eNOS deficiency in mice leads to impaired endothelium-dependent vasorelaxation and a compensatory enhancement of responses to exogenous nitric oxide, demonstrating a gene-dosing effect.
Faraci et al. (1998) studied eNOS deficiency (n=32). eNOS deficiency vs. Wild-type eNOS(+/+) mice was evaluated on Relaxation of carotid arteries in response to 1 microM acetylcholine (p=<0.001). Carotid artery relaxation in response to acetylcholine was impaired in eNOS-deficient mice (55% in +/- and 0% in -/- vs 83% in wild-type, P<0.001), while relaxation to nitroprusside was enhanced.
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