Renal acidification during chronic hypercapnia in the conscious dog.

Abstract

Enhanced renal acidification during chronic hypercapnia (CH) results in transient augmentation in net acid excretion (NAE) (adaptation phase) and persistent acceleration in renal bicarbonate reclamation (adaptation and steady-state phases). The mechanisms responsible for the return of NAE to control values despite persistent acidemia during the steady state phase of CH remain undefined. In addition, it remains unsettled whether the enhancement of renal ammoniagenesis known to occur during the adaptation phase of CH persists during the steady-state phase. Furthermore it is uncertain if the alteration in whole-kidney acidification observed in CH originates from augmentation in the acidification of both proximal and distal nephronal segments. To shed further light on these issues, observations on the profile of the urine acid-base moieties during the adaptive and steady-state phases of CH were carried out in dogs chronically exposed to hypercapnia (10% FiCO2) in an environmental chamber (13 days). Additionally, collecting duct hydrogen ion secretion (CDH+S) was evaluated by employing the U-B PCO2 in alkaline urine in intact unanesthetized dogs with either CH (10% FiCO2) or eucapnia. The balance studies demonstrated that NAE increased in early hypercapnia (4.84 meq/kg body weight, control 3.27 meq/kg body weight, p less than 0.05) and returned to baseline thereafter; by contrast, urine NH+4 which was augmented during the adaptation phase (3.71 meq/kg body weight, control 1.97 meq/kg body weight, p less than 0.05) remained elevated throughout (3.25 meq/kg body weight).(ABSTRACT TRUNCATED AT 250 WORDS)