['To investigate the cellular mechanisms whereby adenosine increases net transendothelial fluid transport by the endothelial cells of the cornea.', 'Rabbit corneas were isolated and the endothelial surface was superfused while thickness was measured with the specular microscope. Cyclic adenosine monophosphate (cAMP) was measured in endothelia from fresh and incubated corneas, and adenylyl cyclase and phosphodiesterase activities were measured in homogenates or the particulate fraction of endothelia from bovine or rabbit. Adenosine, adenosine-receptor agonists, dibutyryl cAMP, forskolin, and phosphodiesterase inhibitors were used to modulate physiological and biochemical parameters.', "Adenosine, N-ethyl(carboxamido)adenosine, dibutyryl cAMP, forskolin, and phosphodiesterase inhibitors all promoted deturgescence of swollen corneas and maintained fresh corneas at lower steady state thicknesses than in controls. These effects were abolished in the presence of ouabain or 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid or after complete removal of HCO3- from the media. Intracellular cAMP was significantly increased by forskolin and phosphodiesterase inhibitors and, to a lesser extent, by agonists. Increases in cAMP concentration declined rapidly with time. Cyclase activity in the bovine tissue was enhanced by agonists and by G-protein activators. Dose-response curves of corneal swelling indicated a greater sensitivity to N-ethyl(carboxamido)adenosine than to the A2 alpha specific agonist CGS 21680."] Does adenosine promote regulation of corneal hydration through cyclic adenosine monophosphate?