The maladaptive renal response to secondary hypocapnia during chronic HCl acidosis in the dog

homeostatic mechanisms of renal origin are re-sponsible for minimizing the alkalemia produced by chronic hypocapnia. Recent observations from this laboratory have demonstrated, however, that the decre-ment in [HCO-], which "protects " extracellular pH in normal dogs, is simply the by-product of a non-specific effect of Paco2 on renal hydrogen ion secre-tion; chronic primary hypocapnia produces virtually the same decrement in plasma [HCO] in dogs with chronic HCI acidosis as in normal dogs (A[HCOfl/ APaco2 = 0.5), with the result that plasma [H+] in animals with severe acidosis rises rather than falls during superimposed forced hyperventilation. This observation raised the possibility that the secondary hypocapnia which normally accompanies metabolic acidosis, if persistent, might induce an analogous renal response and thereby contribute to the steady-state decrement in plasma [HCO] ob-served during HCI feeding. We reasoned that if sus-tained secondary hypocapnia provoked the kidney to depress renal bicarbonate reabsorption, the acute salu-tary effect of hypocapnia on plasma acidity might be seriously undermined. To isolate the possible effects of secondary hypo-capnia from those of the hydrogen ion load, per se, ani-mals were maintained in an atmosphere of 2.6 % CO2 during an initial 8-day period of acid feeding (7 mmol/kg per day); this maneuver allowed Paco2 to be held constant at the control level of 36 mm Hg despite the hyperventilation induced by the acidemia. Steady-state bicarbonate concentration during the A preliminary report of this study was presented in ab-stract form at the American Society of Nephrology Meeting in 1975. Received for publication 21 March 1977 and in revise