Nitric oxide is synthesized from the amino acid I-arginine by a family of enzymes, the nitric oxide synthases. The synthesis of nitric oxide by vascular endothelium is responsible for the vasodilatator tone that is essential for the regulation of blood pressure. NO also contributes to the control of platelet aggregation and the regulation of cardiac contractility. These actions are all mediated by the activation of soluble guanylate cyclase and the consequent increase in the concentration of cGMP in target cells. Several studies suggests that some diseases are related to defects in the generation or action of nitric oxide. Some of the features of septic shock, including hypotension, vascular hyporeactivity, myocardial depression and tissue damage appears to result from excess production of NO. Controlled clinical trials to assess the effects of nitric oxide synthase inhibitors on mortality and morbidity in septic shock seem justified and are already planned.