Transepithelial water flow regulates apical membrane retrieval in antidiuretic hormone-stimulated toad urinary bladder.
Antidiuretic hormone (ADH) increases the osmotic water permeability (Posm) of toad urinary bladder. This increase is believed to be produced by fusion of intracellular vesicles called aggrephores with the granular cell apical plasma membrane. Aggrephores contain intramembrane particle aggregates postulated to be water channels. ADH-stimulated Posm is decreased by osmotic gradient exposure, which is termed flux inhibition. We studied flux inhibition by exposing ADH-stimulated bladders to various osmotic gradients. Osmotic water flow was initially proportional to the applied osmotic gradient, but Posm decreased with time. Ultrastructural and quantitative studies of endocytosis demonstrate that apical membrane retrieval was a direct function of the transepithelial osmotic gradient. Posm remained unchanged when apical membrane retrieval was blocked by incubation of bladders at 2 degrees C, or under low water-flow conditions. These effects were reversed by increases in temperature or the applied osmotic gradient. We conclude that apical membrane retrieval causes the phenomenon of flux inhibition.
D000818:Animals; D001834:Body Water / Q000378:metabolism*; D002024:Bufo marinus; D002462:Cell Membrane / Q000378:metabolism* / Q000648:ultrastructure; D002463:Cell Membrane Permeability / Q000187:drug effects; D003080:Cold Temperature; D003911:Dextrans / Q000378:metabolism; D004705:Endocytosis; D004848:Epithelium / Q000378:metabolism; D005452:Fluoresceins / Q000378:metabolism; D008854:Microscopy, Electron; D008856:Microscopy, Fluorescence; D009995:Osmosis; D001743:Urinary Bladder / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D014667:Vasopressins / Q000494:pharmacology*
D003911:Dextrans; D005452:Fluoresceins; D014667:Vasopressins