Chronic hypercapnia stimulates proximal bicarbonate reabsorption in the rat

Abstract

The hyperbicarbonatemia of chronic respiratory acidosis might be maintained by a reduction in filtration rate or an enhancement of tubular bicarbonate reabsorption. To investigate this question, 12 Munich-Wistar rats were exposed to a 10% CO2 atmosphere for 6-8 d. Chronic respiratory acidosis developed, with arterial pH 7.30 ± 0.01, partial pressure of CO2 (pCO2) 80 ± 2 mmHg, and total CO2 concentration 45 ± 1 mM. Single nephron glomerular filtration rate was normal (42 ± 1 nl/min). Chronic hypercapnia caused absolute proximal reabsorption to be significantly stimulated (1,449 ± 26 pmol/min) as compared with reabsorption previously observed in normal animals (1,075 ± 74 pmol/min) or in animals subjected to acute hypercapnia (1,200 ± 59 pmol/min). This is the first demonstration that proximal bicarbonate reabsorption can be stimulated above normal euvolemic values. When eight animals were subsequently allowed to return toward a normocapnic state (arterial pCO2 46 ± 1 mmHg) over the course of 1-1.5 h, bicarconate reabsorption was still significantly higher (1,211 ± 34 pmol/min) than in similarly alkalotic, normocapnic control groups (994 ± 45 pmol/min). In conclusion, chronic, but not acute, hypercapnia stimulates absolute proximal bicarbonate reabsorption to exceed the level found in normal euvolemic rats.