Nitric oxide (NO) is a powerful vasodilator agent that has been found to be elevated in patients with cirrhosis, and that plays a key role in the pathogenesis of the hemodynamic abnormalities found in these patients. The reasons for this increased NO synthesis are not entirely known, but at least two main mechanisms are involved: shear stress and bacterial-induced NO synthesis. This review focuses on bacterial-induced NO synthesis. Induction of NO synthesis by different cellular populations occurs when proinflammatory cytokines act synergistically, and also by endotoxin. Spontaneous bacterial peritonitis (SBP) is the most dangerous infectious complication arising in patients with cirrhosis and ascites, and it is associated with high serum and ascitic fluid levels of proinflammatory cytokines. A subset of patients in this situation show high levels of serum and ascitic fluid NO levels when SBP is diagnosed, and these patients seem to be predisposed to the development of renal impairment. The increased NO synthesis and associated aggravated vasodilatation may be the reason why patients with SBP show high levels of plasma renin activity, in an attempt to counterbalance this new situation, and that the administration of albumin during the SBP episode significantly reduces the episode-related mortality.