ABSTRACT
Since its discovery as an endothelial-derived relaxant factor (EDRF), nitric oxide (NO) has been demonstrated to play a critical role in numerous physiological processes, as well as in the pathophysiology of many diseases. For example, it is now known that NO is the ubiquitous activator of guanylyl cyclase, resulting in smooth muscle relaxation, platelet reactivity, and central and peripheral neurotransmission. In addition, NO can activate/inhibit a number of other proteins that influence cellular responses. Within a physiological setting, NO release by endothelial cells or nerves contributes to homeostatic processes in every organ system in the body. NO is also released as a primary defense mechanism by immune cells. However, when NO production becomes excessive, its release can contribute to the processes of inflammation and/or cardiovascular dysfunction. The importance of NO as a biological mediator was highlighted by the recent awarding of the Nobel Prize for Physiology and Medicine for description of the interaction between NO and the heme moiety of soluble guanylyl cyclase.
