NO-Dependent Vasorelaxation Is Impaired After Gene Transfer of Inducible NO-Synthase

NO-dependent vasorelaxation is impaired after gene transfer of inducible NO-synthase.

Proinflammatory stimuli produce expression of inducible NO-synthase (iNOS) within blood vessels and are associated with impaired endothelium-dependent relaxation. Gene transfer of iNOS was used to test the hypothesis that expression of iNOS in blood vessels produces impairment of NO-dependent relaxation as well as contraction. An adenoviral vector containing cDNA for murine iNOS, AdCMViNOS, and...

Mechanisms of NO/cGMP-dependent vasorelaxation.

Both cGMP-dependent and -independent mechanisms have been implicated in the regulation of vascular tone by NO. We analyzed acetylcholine (ACh)- and NO-induced relaxation in pressurized small arteries and aortic rings from wild-type (wt) and cGMP kinase I-deficient (cGKI(-/-)) mice. Low concentrations of NO and ACh decreased the spontaneous myogenic tone in wt but not in cGKI(-/-) arteries. Howe...

Absence of Functional Inducible NO Synthase

Inducible NO synthase: role in cellular signalling.

The discovery of endothelium-derived relaxing factor and its identification as nitric oxide (NO) was one of the most exciting discoveries of biomedical research in the 1980s. Besides its potent vasodilatory effects, NO was found under certain circumstances to be responsible for the killing of microorganisms and tumour cells by activated macrophages and to act as a novel, unconventional type of ...

Therapeutic angiogenesis: new indication for endothelial NO synthase gene transfer.

Evidence continues to accumulate on the importance of NO in angiogenesis.1–7 A number of angiogenic substances, including vascular endothelial growth factor (VEGF), stimulate production of NO in endothelial cells.8,9 In vivo biosynthesis of NO is essential for angiogenesis induced by tissue ischemia.3 Angiogenesis is severely impaired in ischemic hindlimb of endothelial NO synthase (eNOS)defici...