Metabolic dependence of the offset of antidiuretic hormone-induced osmotic flow of water across the toad urinary bladder

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Abstract
The elevated osmotic permeability to water induced by antidiuretic hormone (ADH) in the isolated urinary bladder of the toad is rapidly reversed by removal or washout of the ADH. This return to normal water permeability is delayed by the suppression of production of metabolic energy by any of three maneuvers: (i) low temperature (2°C); (ii) inhibition of oxidative phosphorylation (10mm azide or 0.5mm 2,4 dinitrophenol); or (iii) inhibition of glycolysis (10mm iodoacetate or 10mm 2-deoxyglucose). Moreover, exposure to cytochalasin B, 2.1×10−5 m, either before or after initiation of the hormonal effect also delays the return of water permeability to normal following removal of ADH. When considered within constraints imposed by models which predict ADH's action on water permeability to be either via modulation of the fluidity of lipids in the membrane or via the figuration of proteins (“pores”) in the lipid membrane, these observations on the inhibition of the reversal of ADH stimulation of water flow are more consistent with the protein (pore) theory and place limitations on the mechanisms by which proteins in such pores can return to the resting or impermeable state.