Evidence for the implication of endogenous vasopressin in cardiovascular response to central alpha-adrenoceptor stimulation.

To determine the role of endogenous vasopressin (AVP) in cardiovascular response to central alpha-adrenoceptor stimulation, alpha 1-agonist methoxamine or alpha 2-agonist clonidine was administered intracerebroventricularly (ICV) to conscious Long-Evans (LE) rats as well as Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI). In LE rats, ICV methoxamine increased blood pressure (BP) and decreased heart rate (HR), while ICV clonidine caused initial hypertension associated with bradycardia followed by prolonged hypotension with tachycardia. In DI rats, however, ICV methoxamine had no detectable effect on BP and HR, whereas ICV clonidine produced greater hypotension than in LE rats together with less initial bradycardia. Plasma levels of AVP increased 5-15 fold by methoxamine but did not change by clonidine. The intravenous (IV) but not ICV pretreatment with AVP vascular receptor antagonist d (CH2)5 Tyr (Me) AVP significantly attenuated the cardiovascular effects of methoxamine in LE rat, while neither IV nor ICV pretreatment with AVP antagonist modulated the cardiovascular effects of clonidine. These results provide the evidence for the implication of endogenous AVP in the cardiovascular response to central stimulation of alpha-adrenoceptors.