Membrane Transport of CO2 and H2S: No Facilitator Required

The observation that some membranes and epithelia have no demonstrable gas permeability suggested that membrane channels may be involved in CO2 transport. Both aquaporins and Rhesus proteins were reported to serve as pathways for CO2 and H2S. In contrast, we show here that membrane lipid has such high CO2 and H2S permeabilities that the presence of a protein channel does not enhance the flux. Therefore we reconstituted aquaporins into lipid bilayers and used scanning microelectrodes to monitor pH in the immediate vicinity of planar lipid bilayers. The lower limits of lipid bilayer permeabilities to CO2 and to H2S were equal to 3.2±1.6 cm/s[1] and 0.5±0.4 cm/s[2], respectively. We also observed that the CO2 flux through the lipid bilayer decreases several fold when the rate of CO2 formation from HCO3- was not augmented by carbonic anhydrase (CA). Experiments with epithelial cell monolayers grown on permeable support revealed the same result. Inhibition of CA transformed these otherwise highly CO2 permeable cell monolayers into CO2 barriers. Finally we tested the CO2 permeability of the epithelium of the mammalian bladder. It was impermeable to CO2 even after uroplakin knock-out. We found that the lack of intrinsic intracellular CA activity of these epithelial cells hampers the CO2 exchange between blood and urine.[1] A. Missner, P. Kugler, S. M. Saparov, K. Sommer, J. C. Matthai, M. L. Zeidel, P. Pohl, J.Biol.Chem. 2008, 283 25340-25347.[2.] J. C. Mathai, A. Missner, P. Kugler, S. M. Saparov, M. L. Zeidel, J. K. Lee, P. Pohl, Proc.Natl.Acad.Sci.U.S.A. 2009, 106 16633-16638.