DETERMINANTS OF INTRARENAL OXYGENATION .2. HEMODYNAMIC-EFFECTS

To study hemodynamic effects on intrarenal oxygenation, O-2 microelect rodes were inserted into rat kidneys. In a previous study [M. Brezis, Y. Agmon, and F. H. Epstein. Am. J. Physiol. 267 (Renal Fluid Electrol yte Physiol. 36): F1059-F1062, 1994], we showed that tubular metabolis m is a major determinant of intrarenal oxygenation, in part responsibl e for medullary hypoxia observed under basal conditions. Acute hypoten sion (by controlled hemorrhage, aortic ligation, or nitroprusside infu sion) paradoxically increased medullary PO2 (from 21 +/- 2 to 39 +/- 2 mmHg, P < 0.001) while decreasing cortical PO2 (from 46 +/- 2 to 32 /- 3 mmHg, P < 0.001), abolishing corticomedullary gradients of oxygen . Laser-Doppler studies indicated that, while cortical blood flow was reduced during hypotension, medullary blood flow was unchanged or incr eased. The increase in medullary Pot induced by hypotension was abolis hed by prior administration of furosemide, suggesting that during hypo tension, reduced glomerular filtration rate (GFR), distal delivery, an d reabsorption result in decreased oxygen utilization. Acute infusions of atriopeptin III (0.1-1 mu g kg(-1) min(-1)) decreased both cortica l PO2 (from 61 +/- 2 to 55 +/- 2 mmHg, P < 0.001) and medullary PO2 (f rom 15 +/- 1 to 7 +/- 1 mmHg, P < 0.001), consistent with atriopeptin- induced increases in GFR and tubular reabsorptive work. These data sug gest that medullary oxygen availability increases during renal hypoper fusion and may decrease during renal vasodilation.