ABSTRACT
Nitric oxide (NO) is a fascinating ubiquitous molecule with multiple complex roles in biological systems, such as intra and inter cell communications. Endothelial physiology relies on its endothelium derived relaxing factor (EDRF) properties as originally described. NO exhibits physiological vasodilator effects, mediated in part by its binding to the heme group of guanylyl cyclase to produce cGMP that relaxes vascular smooth muscle by lowering cytoplasmic Ca2' levels. So me experiments from several laboratories have very recently established that red blood cells provide a novel vasodilator activity NO mediated in which hemoglobin acts as an O2 sensor and O2-responsive NO signal transducer, thereby regulating both peripheral and pulmonary vascular tone. Haemoglobin through its oxygen binding function adjusts NO bioavailability at the microcirculation and in turn, red blood cells can cause microvessels to dilate or constrict, with S-nitroso-haemoglobin as an intermediate. But other groups demonstrated that SNOHb is not essential for the physiologic coupling of erythrocyte deoxygenation with increased NO bioactivity in vivo. A third group emphasized the role of nitrites and the nitrite reductase activity of hemoglobin as the source of vasodilators in the microcirculation. As blood transfusion in the setting of acute coronary syndromes seemed to be associated with higher mortality, some authors linked those phenomena to the S-nitrosohemoglobin deficiency in banked blood, a mechanism that could explain its loss of physiological activity. In adition to the peripheric actions, the regulatory function of NO on cardiac efficiency also contributes to its key role in the circulation.