V1-receptor mediated GSH efflux by vasopressin from rat hepatocytes

Life Sci. 1992;51(7):507-12. doi: 10.1016/0024-3205(92)90027-m.

Abstract

Vasopression increases sinusoidal efflux of GSH in the perfused rat liver. The mechanism of this effect was studied in the perfused rat liver and in isolated rat hepatocytes. Vasopressin stimulated GSH efflux in both systems and a V1-receptor antagonist (OPC-21268) significantly inhibited the effect of vasopressin suggesting that vasopressin stimulates GSH efflux from rat hepatocytes via V1-receptor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin Receptor Antagonists
  • Animals
  • Biological Transport
  • Cells, Cultured
  • Glutathione / metabolism*
  • Glycogen / metabolism
  • Liver / cytology
  • Liver / drug effects
  • Liver / metabolism*
  • Male
  • Piperidines / pharmacology
  • Quinolones / pharmacology
  • Rats
  • Rats, Inbred Strains
  • Receptors, Angiotensin / metabolism*
  • Receptors, Vasopressin
  • Vasopressins / physiology*

Substances

  • Angiotensin Receptor Antagonists
  • Piperidines
  • Quinolones
  • Receptors, Angiotensin
  • Receptors, Vasopressin
  • Vasopressins
  • OPC 21268
  • Glycogen
  • Glutathione