The conventional wisdom had been that all gases diffuse through all membranes simply by dissolving in the membrane lipid. The first evidence that this view is overly simplistic was our observation over a decade ago that the apical membranes of gastric-gland cells exhibit no permeability to either NH₃ or CO₂. We later showed that expression of aquaporin 1 (AQP1) in Xenopus oocytes causes an increase in CO₂ permeability, assessed by using a microelectrode to monitor the rate at which an exposure to CO₂ causes intracellular pH to fall. A question that then arises is whether the movement of a gas through a channel is ever physiologically relevant. One would expect that the answer might be positive only if: (1) the membrane has a relatively low intrinsic gas permeability and either (2) the rate of gas transport across the membrane is high or (3) the concentration gradient driving diffusion is low. The first evidence of physiological relevance came from Uehlein et al, who found that an AQP1 enhances CO₂ transport in plant cells, a system with a low gradient. The recent data of Endeward et al indicate that AQP1 is responsible for about 60% of CO₂ permeability in human red blood cells, a system with a low intrinsic permeability and a high transport rate. Our preliminary data indicate that AQP1 is similarly responsible for about 65% of the CO₂ permeability of isolated, perfused renal proximal tubules.