Mechanisms of adaptation to chronic respiratory acidosis in the rabbit proximal tubule

The hyperbicarbonatemia of chronic respiratory acidosis is maintained by enhanced bicarbonate reabsorption in the prox-imal tubule. To investigate the cellular mechanisms involved in this adaptation, cell and luminal pH were measured micro-fluorometrically using (2M,7')-bis(carboxyethyl)-(5,6)-carboxy-fluorescein in isolated, microperfused S2 proximal convoluted tubules from control and acidotic rabbits. Chronic respiratory acidosis was induced by exposure to 10 % CO2 for 52-56 h. Tubules from acidotic rabbits had a significantly lower luminal pH after 1-mm perfused length (7.03±0.09 vs. 7.26±0.06 in controls, perfusion rate = 10 nl/min). Chronic respiratory aci-dosis increased the initial rate of cell acidification (dpH1/dt) in response to luminal sodium removal by 63 % and in response to lowering luminal pH (7.4-6.8) by 69%. Chronic respiratory acidosis also increased dpH,/dt in response to peritubular so-dium removal by 63 % and in response to lowering peritubular pH by 73%. In conclusion, chronic respiratory acidosis induces a parallel increase in the rates of the luminal Na/H antiporter and the basolateral Na/(HCO3)3 cotransporter. Therefore, the enhanced proximal tubule reabsorption of bicarbonate in chronic respiratory acidosis may be, at least in part, mediated by a parallel adaptation of these transporters