title: Membrane structural studies of the action of vasopressin.
abstract: Freeze-fracture electron microscopy of the toad urinary bladder indicates that distinctive intramembrane particle aggregates are responsible for the increase in apical membrane water permeability that occurs with vasopressin (VP) stimulation. In unstimulated bladders the aggregates occur in the cytoplasm of the cells in tubular membrane structures now called aggrephores. After stimulation by VP, aggrephores are shuttled to the surface and fuse with the apical membrane. It is suggested by structural observations and by measurements of membrane capacitance that the area of aggregates inserted into the apical membrane is much greater than previously suspected because many aggregates remain in the wall of the fused aggrephores. The area of the aggregates in a stimulated bladder is sufficiently large for these structures to represent an organized array of water channels that mediates the change in apical membrane permeability. Work with antibodies supports the concept that these channels are not always resident in the apical membrane but become inserted only after stimulation by the hormone VP.
mesh_terms: D000818:Animals; D000906:Antibodies; D001001:Anura; D002462:Cell Membrane / Q000502:physiology / Q000648:ultrastructure*; D002463:Cell Membrane Permeability / Q000187:drug effects; D003599:Cytoskeleton / Q000502:physiology / Q000648:ultrastructure; D005614:Freeze Fracturing; D008565:Membrane Proteins / Q000276:immunology / Q000502:physiology; D008855:Microscopy, Electron, Scanning; D001743:Urinary Bladder / Q000502:physiology* / Q000648:ultrastructure; D014667:Vasopressins / Q000502:physiology*
chemical_list: D000906:Antibodies; D008565:Membrane Proteins; D014667:Vasopressins