Abstract
Background NO-sensitive guanylyl cyclase (NO-GC) is the most important effector protein for nitric oxide (NO) and is involved in various physiological processes. Binding of NO stimulates NO-GC up to 200-fold and thereby increases cGMP synthesis. NO is generated by different NO synthases (NOS). In the vasculature, endothelial NOS (eNOS) is involved in the regulation of blood pressure by relaxation of vascular smooth muscle. eNOS is known to be stimulated by shear stress. In addition, NO synthesis is stimulated by vascular endothelial growth factor (VEGF) which acts as one of the most potent stimulators of angiogenesis. Until now the exact signalling pathway of VEGFinduced NO has not been elucidated. S-nitrosylation of protein thiols as well as stimulation of NO-GC with subsequent cGMP increases may underlie the angiogenic effect of VEGF.
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