Role of metabolic CO2 production in the generation of elevated renal cortical PCO2.

Several possible explanations for the elevated CO2 tension observed in structures of the renal cortex have been proposed. The present study was designed to investigate the contribution of renal metabolic CO2 production and removal and the role of incomplete equilibration of the CO2 added to peritubular plasma in an environment devoid of carbonic anhydrase. PCO2 was measured in vivo with PCO2 microelectrodes in early (EP) and late proximal (LP) tubules and stellate vessels (SV) during control conditions and after hyperoncotic albumin, aortic constriction, vanadate, rotenone, or 2,4-dinitrophenol (2,4-DNP) per renal artery, and carbonic anhydrase infusion. In all groups values for PCO2 in EP, LP, and SV sites were indistinguishable but significantly higher than systemic arterial PCO2. PCO2 increased to 71.4 +/- 1.4 mmHg with hyperoncotic albumin and to 87.0 +/- 1.8 mmHg after 2,4-DNP (P less than 0.001). During aortic constriction, vanadate infusion, and rotenone per renal artery, PCO2 fell to 53.7 +/- 0.9, 55.2 +/- 2.5, and 57.3 +/- 1.3, respectively (P less than 0.001). Renal O2 consumption decreased significantly after rotenone (-38.1 +/- 5.6 to -13.3 +/- 2.7 mumol X min-1 X kg-1) and increased significantly after 2,4-DNP (-35.7 +/- 5.9 to -75.9 +/- 6.9 mumol X min-1 X kg-1). These findings demonstrate that renal energy utilization and metabolic CO2 production represents an important source of renal cortical PCO2. Carbonic anhydrase infusion resulted in a decrease in PCO2 to 58.2 +/- 1.2 mmHg (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)