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Carbonic Anhydrase II and Alveolar Fluid Reabsorption during Hypercapnia

¹ Division of Pulmonary and Critical Care Medicine, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois

Correspondence and requests for reprints should be addressed to Jacob I. Sznajder M.D., Division of Pulmonary and Critical Care Medicine, 240 E. Huron, McGaw M-300, Northwestern University, Feinberg School of Medicine Chicago, IL 60611. E-mail: j-sznajder{at}northwestern.edu

Carbonic anhydrase II (CAII) plays an important role in carbon dioxide metabolism and intracellular pH regulation. In this study, we provide evidence that CAII is expressed in both type I (AECI) and type II (AECII) alveolar epithelial cells by RT-PCR and Western blotting in freshly isolated rat cells. These results were further confirmed by double immunostaining with CAII antibodies and AECI- or AECII-specific markers in freshly isolated alveolar epithelial cells and rat lung tissues. Inhibition of CAII by acetazolamide or methazolamide delayed the decrease in the intracellular pH observed during hypercapnia in cultured AECI, AECII, and AECI-like cells. In an isolated-perfused rat lung model, alveolar fluid reabsorption significantly decreased during high CO₂ exposure, which was not prevented by carbonic anhydrase inhibition. Thus, we provide evidence that CAII is expressed in rat alveolar epithelial cells and does not regulate lung alveolar fluid reabsorption during hypercapnia.

Key Words: carbonic anhydrase II • rat alveolar epithelial cells • intracellular pH • alveolar fluid clearance • hypercapnia

CLINICAL RELEVANCE This is the first report showing that carbonic anhydrase (CA) protein is expressed in type I epithelial cells and in which this activity was measured. Inhibition of CA activity in the alveolar epithelium does not have an effect on alveolar fluid reabsorption.

 

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