The recent discovery of ‘aquaporins’, a large family of membrane proteins that function as highly selective water channels has drawn attention to their role in physiology and in several human diseases that involve rapid water transport, and have identified them as potential targets for therapeutic intervention. At least ten aquaporins (AQPs), numbered 0 through 9, have been identified from various mammalian tissues. The finding of homologous genes in amphibians, insects, and bacteria highlights the evolutionary conservation and thus probable importance of these proteins. Aquaporins seem to be most highly expressed in tissues whose function involves rapid water movement across the cell membrane. Several recent studies have identified the specific roles for aquaporins in well-recognized physiologic processes and diverse pathophysiologic disorders common in the practice of clinical medicine. For example, mutations in AQP0 result in congenital cataracts and mutations in AQP2 (vasopressin-regulated kidney water channel) result in a severe form of nephrogenic diabetes insipidus. In addition, knockout mice studies with selective deletions of various aquaporins suggest a role for AQP1 and AQP3 in kidney and AQP4 in brain and colonic fluid transport. Deletion of AQP5, the apical membrane water channel in the salivary gland, caused defective saliva production. Whereas, deletion of AQP1 or AQP5 water channels resulted in a significant decrease in airspace-capillary water permeability.