Purpose of review: Nitric oxide is a potent, endogenous vasodilator that regulates systemic blood pressure and renal function, among other functions. The bioactivity of nitric oxide is reduced by superoxide, a major reactive oxygen species. Overproduction of superoxide and other related reactive oxygen species resulting in oxidative stress reduces the biological effects of nitric oxide. Though both of these highly reactive species have distinct roles in other pathways, their interaction is emerging as a major regulatory factor in normal and pathological renal function. The purpose of this review is to highlight the recent studies on oxidative stress and nitric oxide in the kidney, focusing on their interaction in normal and pathological conditions.
Recent findings: Studies have focused on pro-oxidant pathways and nitric oxide defense systems in normal and pathological conditions. The oxidant potential of uncoupled nitric oxide synthases is gaining interest as a pro-oxidant system. Both animal and clinical studies have attempted to identify strategies to intervene at various stages of the oxidant-nitric oxide pathways to improve function during renal failure.
Summary: Several new approaches and provocative findings have emerged over the last year. A regulatory role for nitric oxide in the control of the renal microcirculation and as a participant in tubule function is further described. New information of the cause and possible prevention of acute and chronic renal failure has also been produced in the last year. These advances demonstrate the value of research in the normal and pathological roles of oxidative stress and nitric oxide in the kidney.