Purpose of review: The regulatory role of nitric oxide for tissue oxygen availability involves both oxygen delivery, through regulation of vascular tone, and oxygen consumption, through interference with mitochondrial respiration and tubular transport capacity. This review highlights recent findings regarding mechanisms of dysfunctional nitric oxide bioavailability in the kidney and the implications for oxygen availability and mitochondrial respiration.
Recent findings: It has been revealed that nitric oxide has several ways to influence and regulate kidney function during normal physiological conditions and that it is also involved in many of the mechanisms resulting in altered kidney function during disease. Recent reports show that nitric oxide regulates kidney oxygenation by influencing both oxygen utilization and supply.
Summary: Increasing evidence has accumulated during recent years for a dysfunctional nitric oxide system resulting in altered kidney oxygenation in several pathological conditions, which contributes to the development of kidney failure. We presently have extensive knowledge regarding the interplay between nitric oxide, oxygenation and kidney function; however, more effort is needed to clarify how dysfunctional nitric oxide regulation progresses to tissue hypoxia and kidney failure in various conditions, in order to identify potential therapeutic targets and develop strategies to prevent or alleviate these adverse effects and maintain adequate kidney function.