Endogenous opioid peptide inhibition of the central actions of angiotensin

Effects of endogenous opioid peptides (leucine5-enkephalin; methionine5-enkephalin; and beta-endorphin) and morphine on isoleucine5-angiotensin II (All)-stimulated increase in plasma vasopressin concentration, blood pressure and drinking behavior were characterized in conscious rats. Plasma vasopressin concentration, drinking frequency and latency were measured 90 sec after intracerebroventricular (i.v.t.) All in animals pretreated with enkephalins, beta-endorphin or morphine, i.v.t. Vasopressin was measured by radioimmunoassay. A consistent dose-related, naloxone-sensitive inhibition of the All-stimulated increase in plasma vasopressin concentration and drinking behavior (frequency) occurred after enkephalins, beta-endorphin or morphine. beta-Endorphin and morphine were longer acting and more potent than enkephalins. In other experiments, All (i.v.t.) pressor activity, drinking volume and latency were measured at hourly intervals after opiates, i.v.t. The All-stimulated increase in mean blood pressure and drinking volume were inhibited by endogenous opioid peptides and morphine, i.v.t. Naloxone prevented opiate inhibition of the All pressor response. Endogenously synthesized opiates may modulate All activity as naloxone potentiated the pressor response and decreased water consumption after All, i.v.t. Continuous i.v. infusion of leucine-enkephalin did not affect All drinking or pressor activity, indicating a central nervous system site of inhibition. Opiate inhibition of the central actions of All appeared independent of sedation; head shakes or wet dog shakes occurred at effective doses of enkephalins. Naloxone did not affect basal blood pressure or plasma vasopressin concentration. Endogenous opioid peptides may modulate the central actions of angiotensin II affecting blood pressure and hydration.