Regulation of acid-base equilibrium in chronic hypocapnia. Evidence that the response of the kidney is not geared to the defense of extracellular (H+).

Abstract

A C T It is generally believed that the reduc- tion in plasma [HCO3] characteristic of chronic hypo- capnia results from renal homeostatic mechanisms de- signed to minimize the alkalemia produced by the hypo- capneic state. To test this hypothesis, we have induced chronic hypocapnia in dogs in which plasma [HCOs] had previously been markedly reduced (from 21 to 15 meq/liter) by the prolonged feeding of HCl. The Paco2 of chronically acid-fed animals was reduced from 32 to 15 mm Hg by placing the animals in a large environ- mental chamber containing 9% oxygen. In response to this reduction in Paco2, mean plasma [HCO3] fell by 8.6 meq/liter, reaching a new steady-state level of 6.4 meq/liter. This decrement in plasma [HCO3] is almost identical to the 8.1 meq/liter decrement previously ob- served in normal (nonacid-fed) animals in which the same degree of chonic hypocapnia had been induced. Thus, in both normal and HCl-fed animals, the renal response to chronic hypocapnia causes plasma [HCO3] to fall by approximately 0.5 meq/liter for each millimeter of Hg reduction in C02 tension.