Key result
Aortas from eNOS knockout mice showed increased sensitivity to the nitric oxide donor SPER-NO compared to wild-type mice (pEC50 7.30 vs 6.56, P<0.05), indicating up-regulation of sGC-cGMP signaling.
Population
Mouse thoracic aorta from wild type and NO synthase knockout animals
Comparison
Pharmacological agents including NO donor, sGC… vs Wild type mice aortas, or baseline responses…
Design
Preclinical
Authors
Loading...
Indicates selective NO-sGC sensitization in eNOS deficiency; leaves open relevance to human endothelial dysfunction or therapy.
Absolute Event Rate: 7.3% vs 6.56%
p-value: p=<0.05
Vessels from eNOS knockout mice show increased sensitivity to nitric oxide, suggesting specific up-regulation of sGC-cyclic GMP signalling as a mechanism for dynamic regulation of NO bioactivity.
Hussain et al. (1999) studied this question. eNOS knockout vs. Wild type (WT) mice was evaluated on Potency of SPER-NO (pEC50) (p=<0.05). Aortas from eNOS knockout mice showed increased sensitivity to the nitric oxide donor SPER-NO compared to wild-type mice (pEC50 7.30 vs 6.56, P<0.05), indicating up-regulation of sGC-cGMP signaling.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: