Effects of vasopressin on phosphoinositide hydrolysis and myocardial contractility

The effects of vasopressin on phosphoinositide hydrolysis, ventricular contractility and adrenoceptor-mediated inotropy were studied in the rabbit. Vasopressin caused an accumulation of [3H]inositol monophosphate in ventricular slices prelabelled with myo-[3H]inositol, whereas it elicited a small but definite negative inotropic effect. In addition, vasopressin attenuated the positive inotropic effect elicited via alpha 1- and endothelin receptors without affecting the beta-adrenoceptor-mediated effect. The nonpeptide-selective V1 receptor antagonist OPC 21268 (a quinolinone derivative) inhibited the vasopressin-induced accumulation of [3H]inositol monophosphate. The present results indicate that vasopressin stimulates phosphoinositide hydrolysis via V1 receptors, but inhibits force and the alpha 1-mediated positive inotropic effect in the rabbit ventricular myocardium.