Published ahead of print on August 9, 2007, doi:10.1165/rcmb.2007-0121OC Am. J. Respir. Cell Mol. Biol., Volume 38, Number 1, January 2008, 32-37 A more recent version of this article appeared on January 1, 2008
Submitted on April 5, 2007 Carbonic Anhydrase II and Alveolar Fluid Reabsorption During HypercapniaJiwang Chen1,1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA * To whom correspondence should be addressed. 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.
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