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- W2160992728 endingPage "838" @default.
- W2160992728 startingPage "825" @default.
- W2160992728 abstract "Ruthenium-derived complexes have emerged as new nitric oxide (NO) donors that may help circumvent the NO deficiency that impairs vasodilation. NO in vessels can be produced by the endothelial cells and/or released by NO donors. NO interacts with soluble guanylyl-cyclase to produce cGMP to activate the kinase-G pathway. As a result, conductance arteries, veins and resistance arteries dilate, whereas the cytosolic Ca 2+ levels in the smooth muscle cells decrease. NO also reacts with oxygen or the superoxide anion, to generate reactive oxygen species that modulate NO-induced vasodilation. In this article, we focus on NO production by NO synthase and discuss the vascular changes taking place during hypertension originating from endothelial dysfunction. We will describe how the NO released from ruthenium-derived complexes enhances the vascular effects arising from failed NO generation or lack of NO bioavailability. In addition, how ruthenium-derived NO donors induce the hypotensive effect by vasodilation is also discussed." @default.
- W2160992728 created "2016-06-24" @default.
- W2160992728 creator A5011586813 @default.
- W2160992728 creator A5037075429 @default.
- W2160992728 creator A5056776784 @default.
- W2160992728 creator A5082830013 @default.
- W2160992728 date "2014-05-01" @default.
- W2160992728 modified "2023-10-13" @default.
- W2160992728 title "Enhancing vascular relaxing effects of nitric oxide-donor ruthenium complexes" @default.
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