Permeability pathways for non-electrolytes through Bufo bufo gall-bladder

Pflugers Arch. 1975 Mar 26;355(3):267-71. doi: 10.1007/BF00583689.

Abstract

Amphotericin B treatment increases the thiourea, D-xylose and mannitol fluxes and lowers those of urea, N-methyl-urea, acetamide, formamide, and N-N'-dimethyl-thiourea. The degree of flux inhibition is related to the cellular permeability of these compounds. Most probably Amphotericin B increases the permeability of all those molecules across the luminal plasma membrane, but simultaneously elicits a cellular swelling, which reduces the diffusion across the lateral plasma membranes. This effect masks the polyene effect especially for molecules showing a mainly cellular permeation pathway such as amides and lipid soluble molecules.

MeSH terms

  • Acetamides / metabolism
  • Amphotericin B / pharmacology
  • Animals
  • Bufo bufo
  • Cell Membrane Permeability* / drug effects
  • Female
  • Formamides / metabolism
  • Gallbladder / drug effects
  • Gallbladder / metabolism*
  • Humans
  • Mannitol / metabolism
  • Molecular Conformation
  • Mucous Membrane / metabolism
  • Serous Membrane / metabolism
  • Urea / analogs & derivatives
  • Urea / metabolism
  • Xylose / metabolism

Substances

  • Acetamides
  • Formamides
  • Mannitol
  • Amphotericin B
  • Urea
  • Xylose