Analysis of the determinants of renal cortical PCO2.
Recent studies employing Pco2 microelectrodes demonstrated CO2 tensions in the renal cortex (60-65 mmHg) that are significantly greater than systemic arterial Pco2. Three sources for CO2 generation have been proposed: 1) luminal production from H+ and HCO-3,2) addition of HCO-3 to peritubular plasma with disequilibrium for H+/HCO-3/CO2, and 3) metabolic CO2 production. None of these mechanisms alone can adequately explain the findings. The purpose of this study was to examine mechanisms of elevated renal cortical Pco2 generation and maintenance by developing a mathematical model for the reaction and transport processes involved in proximal tubule HCO-3 reabsorption. Steady-state calculations of pH, Pco2, and [HCO-3] for luminal, cellular, and vascular compartments employing simple mass balance considerations are presented. Besides exploring the role of metabolic CO2 production in the genesis and maintenance of elevated renal cortical Pco2, we also propose and examine the additional mechanism of diffusive transfer of CO2 between renal cortical venular and afferent arteriolar capillaries. Our results show that the required magnitude of either metabolic CO2 production or diffusive CO2 transfer alone is large (3 mmol/liter RBF). However, vascular-vascular exchange of CO2 gas in combination with accepted levels of metabolic CO2 production can adequately explain the findings of an elevated renal cortical Pco2 of approximately 65 mmHg as measured experimentally in vivo.
D000042:Absorption; D001639:Bicarbonates / Q000378:metabolism; D002245:Carbon Dioxide / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism*; D007672:Kidney Cortex / Q000378:metabolism*; D007687:Kidney Tubules, Proximal / Q000378:metabolism; D008954:Models, Biological; D010313:Partial Pressure
D001639:Bicarbonates; D002245:Carbon Dioxide