EFFECT OF HYPERCAPNIC ACIDOSIS ON RENAL WATER-EXCRETION IN THE DOG

Impaired renal water excretion has been observed in patients with hypercapnic acidosis. We therefore induced hypercapnic acidosis (P(CO)2, 25 to 70 mm Hg, P<0.001; pH, 7.43 to 7.05, P<0.001) in anesthetized dogs undergoing water diuresis. Renal perfusion pressure was kept constant in all studies. Hypercapnic acidosis resulted in a significant fall in mean arterial pressure (MAP, 147 to 128 mm Hg, P<0.001) and significant increases in cardiac output (3.9 to 4.7 liters/min, P<0.05). Renal vascular resistance (RVR, 0.49 to 0.76 mm Hg/ml/min, P<0.01) and filtration fraction (FF, 0.27 to 0.33, P<0.005) rose as GFR remained constant. The increases in RVR and FF were abolished by renal denervation. An antidiuresis, however, occurred with hypercapnic acidosis in both innervated (U(Osm), 107 to 510 mOsm/kg H2O, P<0.001) and denervated (U(Osm), 85 to 379 mOsm/kg H2O, P<0.001) kidneys. This antidiuresis was associated with a significant increase in radioimmunoassayable arginine vasopressin (AVP, 0.2 to 3.4 μU/ml, P<0.005). In a separate group of dogs, pevention of the fall in MAP during hypercapnic acidosis with a norepinephrine infusion did not prevent either an antidiuresis (U(Osm), 100 to 465 mOsm/kg H2O, P<0.005) or an increase in AVP (0.2 to 2.8 μU/ml, P<0.005). Hypophysectomy eliminated hypercapnic acidosis associated increases in AVP (0.1 to 0.1 μU/ml, NS) and U(Osm) in denervated (75 to 86 mOsm/kg H2O) but not innervated (81 to 133 mOsm/kg H2O, P<0.05) kidneys. In another group of hypophysectomized dogs, hypercapnic acidosis did not potentiate the antidiuretic effect of exogenous AVP. These results indicate that hypercapnic acidosis results in an antidiuresis predominately through release of AVP, and this release of AVP occurs independent of a decrease in MAP. Hypercapnic acidosis also exerts an AVP-independent antidiuretic effect mediated by renal nerves.