Aquaporins (AQs) increase cell membrane CO2 diffusivity, and it has been proposed that they may serve as transmembrane channels for CO2 and other small gas molecules. In addition, it has been hypothesized that voltage-gated H+ channels located on the apical membrane of the alveolar epithelium contribute to CO2 elimination by the lung. To test whether these membrane proteins contribute to CO2 elimination in vivo, we measured CO2 exchange in buffer- and blood-perfused rabbit lungs before and after addition of 0.5mM ZnCl2, an inhibitor of both AQ-mediated CO2 diffusion and voltage-gated H+ channels. For comparison, red cell and lung carbonic anhydrases (CAs) were inhibited by 0.1mM methazolamide. ZnCl2 had no effect on CO2 exchange when inspired CO2 was altered between 2% and 5% in 5-min intervals. Pulmonary vascular and airway resistances were not altered by ZnCl2. In contrast, methazolamide inhibited CO2 exchange by 30% in buffer-perfused lungs and by 65% in blood-perfused lungs. Exhaled NO concentrations were unaffected by ZnCl2 or by CA inhibition. Lung capillary gas exchange modelling shows that under normal resting conditions it would be necessary to reduce the alveolar–capillary membrane CO2 diffusion capacity by >90% to lower CO2 elimination by 10%. Therefore we conclude that red cell and lung AQs and voltage-gated H+ channels in the alveolar epithelium contribute minimally to normal physiological CO2 elimination.

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