Review An Effective Transmitter: Nitric Oxide

The vascular endothelium is an active participant in the regulation of vascular tone and blood flow. Its dysfunction leads to a reduction in the synthesis and release or an excessive degradation of nitric oxide (NO). NO, an endothelium-derived relaxing factor (EDRF) is released by different types of cells of the body. Recently the results of many experiments and clinical studies confirm that NO is a primary physiological transmitter with a wide spectrum of physiological and pathophysiological effects. NO is synthesized in the endothelial cells from the amino L-arginine by nitric oxide synthases with stimulation by acethylcholine, bradykinin, substance P, thrombin, ADP, ATP, calcium thromboxane A2 histamine, endothelin and aggregating platelets. Its release can be altered also by mechanical forces such as shear stress, blood pressure and pulsatile stretch. No, by relaxing vascular smooth mucle by activating guanylate cyclase is responsible for the vasodilatator tone that is essential for the regulation of blood pessure. It also contributes to the control of the function of platelets and leukocyts. A deficiency in the activity of NO may be the mechanism of diminished via dilation in patients with atherosclerosis, so ischemic heart disease, hyproxia, heart failure, diabetes mellitus and hypertension. Organic nitrates which are metabolized to NO or S-nitrosothiol at cellular level induce vasodilatation by activiting guanlylate cyclase, but they have no effect on the very small vessels such as endogeneous NO. Future experiments and clinical studies will determine the place and the effectiveness of new NO donors and NO-synthase inhibitors in preventing atherosclerosis, ischemic heart disease, hypertension, platelet dysfunction and other diseases.