OPIATE REGULATION OF ANGIOTENSIN-INDUCED DRINKING AND VASOPRESSIN RELEASE

  • 1 January 1981
    • journal article
    • research article
    • Vol. 217  (3) , 630-637
Abstract
In rats, intracerebroventricular (i.v.t) administration of endogenous opioid peptides inhibited angiotensin II-stimulated increase in plasma vasopressin concentration and drinking behavior. Naloxone and naltrexone were used to evaluate the effect of opiate receptor blockade on angiotensin drinking behavior. Both antagonists reduced the amount of water consumed and number of animals drinking in response to angiotensin II (i.v.t.). The time to onset of drinking was unaffected. Leu5-enkephalin inhibition of angiotensin-stimulated release of vasopressin was also studied. Changes in plasma vasopressin concentration with time (5, 45, 90, 150 and 300 s) were measured after a single i.v.t. injection of angiotensin II (50 ng), with and without pretreatment with leu5-enkephalin (100 .mu.g i.v.t.). Vasopressin was measured by radioimmunoassay. The onset of vasopressin release occurred 5-45 s after angiotensin, reaching a peak response between 45-90 s. Leu5-enkephalin did not affect the onset but reduced the peak response to angiotensin (P < 0.05). Saralasin, i.v.t., abolished angiotensin-stimulated increase in plasma vasopressin concentration and prevented the residual, but significant, increase in plasma vasopressin concentration in angiotensin-treated rats given enkephalin. Angiotensin stimulates release of vasopressin by interaction with specific, saralasin-sensitive, receptors; leu5-enkephalin inhibits angiotensin release of vasopressin; and an endogenously synthesized opiate ligand(s) may affect angiotensin drinking behavior.