Pharmacological doses of atrial natriuretic peptide ameliorate the acute renal dysfunction induced by systemic hypoxemia.

The acute renal effects of systemic hypoxemia and the ability of atrial natriuretic peptide (ANP) to reverse these effects were assessed in seven anesthetized and mechanically ventilated adult rabbits. Throughout the experiment, arterial pH, PaCO2 and HCO3 remained unchanged. Hypoxemia induced a significant increase in rabbit-ANP plasma levels from 151 +/- 26 to 246 +/- 65 pg/ml. During the normoxemic period (PaO2 = 131 +/- 12 mm Hg), glomerular filtration rate (GFR), renal blood flow (RBF), renal vascular resistance (RVR) and urinary sodium excretion (UNaV) were similar in both kidneys. The subsequent hypoxemic period (PaO2 = 30 +/- 1 mm Hg) caused a decrease in right and left kidney function: GFR, -26 +/- 5 and -29 +/- 6%; RBF, -17 +/- 9 and -29 +/- 8%; RVR, +28 +/- 16 and +59 +/- 30%; urine flow rate, -38 +/- 6 and -36 +/- 6%; and UNaV, -51 +/- 7 and -50 +/- 7%, respectively. Human-ANP infusion in the left renal artery (100 ng/min) during sustained systemic hypoxemia induced a significant improvement in GFR (+57 +/- 18%), RBF (+21 +/- 8%), RVR (-20 +/- 7%), urine flow rate (+151 +/- 27%) and UNaV (+270 +/- 48%) in the left experimental kidney, as compared with the preceding hypoxemic period. In contrast, the function of the right control kidney remained impaired.