Nitric oxide and hemoglobin interactions in the vasculature.
As an endothelium-derived relaxing factor, nitric oxide (NO) maintains blood flow and O2 transport to tissues. Under normal conditions a delicate balance exists in the vascular system between endothelium-derived NO, an antioxidant, and the pro-oxidant elements of the vascular system, O-2, and peroxynitrite (a by-product of the reaction of NO and superoxide); in addition there is a balance between neurogenic tonic contraction and NO-mediated relaxation. The former balance can be disrupted in favor of peroxynitrite and hydrogen peroxide under the conditions of ischemia/reperfusion. This review suggests that NO may be beneficial, not only in terms of its new potential in improving O2 transport without accompanying significant increase in tissue blood flow, but also in its ability to suppress the prooxidative reagents of the vascular systems. These include NO-mediated inhibition of transendothelial migration by leukocyte and the antioxidative effects of NO with regard to ischemia/reperfusion; the relevance of these hypotheses to systemic administration of NO donors is discussed.
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism*; D006454:Hemoglobins / Q000737:chemistry / Q000378:metabolism*; D006801:Humans; D007511:Ischemia / Q000503:physiopathology; D007962:Leukocytes / Q000502:physiology; D009569:Nitric Oxide / Q000097:blood / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D005996:Nitroglycerin / Q000494:pharmacology; D010100:Oxygen / Q000737:chemistry / Q000378:metabolism; D015424:Reperfusion; D013481:Superoxides / Q000378:metabolism