Regulation of water permeability in toad urinary bladder at two barriers.
The effects of prostaglandin synthesis inhibition by naproxen were studied in toad bladder. Luminal membrane water permeability was evaluated both by the frequency of intramembranous particle aggregates in granular cell luminal membrane and by direct assessment of the rate of change of cell volume during perfusion of an anisosmotic solution. Total tissue water permeability was assessed by transbladder osmotic water flow. Inhibition of prostaglandin synthesis caused luminal membrane water permeability to increase much more than expected from tissue permeability measurements. The addition of a very low dose of antidiuretic hormone (ADH) (0.125 mU/ml) during prostaglandin synthesis inhibition increased luminal membrane water permeability to the same level as maximal stimulation with ADH, while tissue water permeability failed to increase proportionately. The results imply the presence of a regulatable barrier to water movement across toad bladder that is distal to the luminal membrane and subject to control by either prostaglandins or ADH.
D000818:Animals; D001834:Body Water / Q000378:metabolism*; D002024:Bufo marinus; D009288:Naproxen / Q000494:pharmacology; D009994:Osmolar Concentration; D009995:Osmosis; D010539:Permeability; D001743:Urinary Bladder / Q000166:cytology / Q000378:metabolism*; D014667:Vasopressins / Q000494:pharmacology
D014667:Vasopressins; D009288:Naproxen