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

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.