In artificial lipid bilayer membranes, the ratio of the water permeability coefficient (Pd (water)) to the permeability coefficient of an arbitrary nonelec-trolyte such as n-butyramide (.Pd (n-butyramide)) remains relatively constant with changes in lipid composition and temperature, even though the individual Pd’s increase more than 100-fold. I propose that this is a general rule that also holds for the lipid bilayers of cells and tissues, and that therefore if Prf(water)/Prf(solute) greatly exceeds the value found for artificial lipid bilayers (where "solute" is a molecule, such as 1,6 hexanediol or n-butyramide, that crosses the cell membrane by a solubility-diffusion mechanism without the aid of a special transporting system), then water crosses the cell membrane via aqueous pores. Applying this criterion to the toad urinary bladder, we find that even in the unstimulated bladder, water probably crosses the luminal membrane primarily through small aqueous pores, and that this is almost certainly the case after antidiuretic hormone (ADH) stimulation. I suggest that ADH stimulation ultimately leads either to formation (or enlargement) of pores, by the rearrangement of preexisting sub-units, or to an unplugging of these pores.
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