Population
Wild-type (WT) mice and endothelial NO synthase knockout (eNOS(-/-)) mice (aortic segments)
Comparison
Sodium nitroprusside and N-Nitro-L-arginine vs Wild-type (WT) mice
Design
Preclinical
Authors
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May indicate compensatory sGC sensitization in chronic NO deficiency; hypothesis-generating in mice and leaves open human relevance.
Chronic deficiency of endothelial NO in eNOS(-/-) mice restores the NO sensitivity of soluble guanylyl cyclase (sGC) and enhances vascular smooth muscle relaxation in response to nitrovasodilators without altering sGC expression.
Brandes et al. (2000) studied this question.
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