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A B S T R A CT The effect of prostaglandin Ei (PGEi) on osmotic water flow across toad bladder and cyclic AMP content of the mucosal epithelial cells has been determined under basal conditions and in the presence of either theophylline or antidiuretic hormone (ADH). Under basal conditions and with PGE, concentrations from 10 to 10' M no evidence of stimulation of water flow was observed, and with 10' M PGEi a significant inhibition was found. Cyclic AMP content under control conditions was 8 pmol/mg protein. It was 9 at 10' M PGEi, 13 at 10' M, 16 at 10' M, and 23 at 10' M. In the presence of theophylline, 10' and 10V M PGE1 inhibited the theophylline-induced water flow as expected. In contrast, 10' and adenylate cyclase controlling water flow. Thus the increase in cyclic AMP content in response to PGE, is not derived from this enzyme. Thus the stimulation of water flow by PGE1 in the presence of theophylline is thought to be caused by cyclic AMP spilling over from one compartment to the water flow compartment. No evidence was obtained to directly suggest spillover into the sodium transport compartment. Furthermore evidence is discussed to suggest that most of the cyclic AMP generated in the tissue does not originate from the enzyme controlling sodium transport. As cyclic AMP-stimulated water flow and sodium transport are thought to occur in one cell type, the granular cells, distinct pools of cyclic AMP are thought to be present in one and the same cell type. Thus one pool controls water flow and one controls sodium transport. With high concentrations of PGE1 in the presence of theophylline or high concentrations of ADH, the adenylate cyclase responsible for water flow is inhibited. However, PGEi can stimulate a tissue adenylate cyclase to sufficiently high levels that cyclic AMP spills over into the "water flow compartment" and thus stimulates water flow.

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