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pubmed:abstractText |
The frog urinary bladder undergoes, in some conditions, a marked increase of its water permeability when incubated in hypertonic media. This increase was observed with various nonpermeant solutes. It seems to result from the shrinkage of an osmo-sensitive compartment of the tissue, probably the epithelial cells. Many similarities were found between this effect and the physiological increase in water permeability (hydrosmotic response) elicited by antidiuretic hormone (ADH): both were dependent on the physiological state of the animals, and although the response was slower after hyperosmolar than after hormonal challenge, the patterns of response were similar, and in both cases markedly dependent on bathing solution temperature. Norepinephrine and prostaglandin E(1), which in this tissue reduce the hydrosmotic action of ADH, presumably by inhibiting the adenyl cylase also reduced the effect of hyperosmolarity. Conversely this effect was potentiated by incubation in the presence of oxytocin, exogenous cyclic AMP, and theophylline, conditions in which the intracellular concentration of cyclic AMP is increased. These data demonstrate that the response to hyperosmolarity is elicited, at least partly, by mechanisms also involved in the physiological hydrosmotic response to ADH.
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