Is Vasopressin-Stimulated Inositol Lipid Breakdown Intrinsic to the Mechanism of Ca2+-Mobilization at V1 Vasopressin Receptors?

Research output: Contribution to journalArticlepeer-review

Authors

Colleges, School and Institutes

External organisations

  • Department of Biochemistry
  • University of Birmingham

Abstract

A role for Ca2+ in the mechanism whereby vasopressin stimulates liver and smooth muscle is suggested by the observations that aortic contraction and hepatic glycogenolysis are diminished in Ca2+-free media and that the latter effect can be mimicked by the Ca2+ ionophore A23187. This chapter describes that vasopressin-stimulated inositol lipid breakdown may have a role in the mechanism, whereby V1-receptor activation provokes Ca2+-mobilization in stimulated cells. There have been a number of suggestions as to how inositol lipid breakdown might be coupled to Ca2+-mobilization in stimulated cells. The chapter suggests that vasopressin might be a neurotransmitter in the central nervous system (CNS). It is interesting to note that V1-receptors have been identified in hippocampal neurons of the rat and latest studies have shown that vasopressin stimulates the accumulation of inositol phosphates in rat hippocampal slices and rat sympathetic ganglia. Therefore, it seems likely that information on the mechanism of action of V1-receptors in peripheral tissues may also help understand the actions of vasopressin in the CNS.

Details

Original languageEnglish
Pages (from-to)405-411
Number of pages7
JournalProgress in brain research
Volume60
Issue numberC
Publication statusPublished - 1 Jan 1983

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