Intrarenal oxygen and hypertension.

The kidney has a unique environment that results in relatively low tissue oxygen tension (Po2). However, recent studies have shown that renal hypoxia is more severe during hypertension and may reflect changes in the way O2 is used. The present review summarizes studies that explore the relationship between renal oxygen tension (Po2), oxygen consumption and hypertension. More recent studies suggest that oxidative stress accompanying hypertension, rather than the elevated blood pressure per se reduces Po2. The Po2 in various sections of the kidney often reflects the level of oxygen consumption, which varies depending on the sites of Na+ reabsorption, a process that consumes nearly 90% of total renal oxygen. The efficient use of oxygen for the transport of Na+ in the kidney is reduced during hypertension, which may contribute to the resulting hypoxia. Conversely, the defect in renal oxygen usage due to oxidative stress may exacerbate hypertension in animal models. The goal of many of these studies is to determine the impact of renal hypoxia in the generation of hypertension.