DETERMINANTS OF INTRARENAL OXYGENATION .1. EFFECTS OF DIURETICS

To study renal cortical and medullary oxygen tensions, we used sensitive Clark-type O-2 microelectrodes, inserted by micromanipulators into the cortex and medulla of kidneys of anesthetized rats. As previously reported, under basal conditions, medullary Po-2 was significantly lower than cortical Pot. Furosemide, which inhibits reabsorptive transport in the medullary thick ascending limb, increased medullary Po-2 from 16 +/- 4 to 35 +/- 4 mmHg (P < 0.0005) without altering cortical Po-2. This effect, reproduced by ethacrynic acid and bumetanide, was selective for loop diuretics and was directly due to decreased tubular O-2 consumption, since medullary blood flow was remarkably reduced by furosemide (-28 +/- 6% from baseline, P < 0.0001, as measured by a laser-Doppler probe). By contrast, acetazolamide, which decreases proximal tubule metabolism, selectively increased cortical Po-2. These data are, in general, consistent with tubular metabolism as a major determinant of intrarenal oxygenation and suggest, in particular, that medullary reabsorptive work is at least in part responsible for renal medullary hypoxia.