d-ala(2)-mephe(4)-met(0)-ol-enkephalin and 7-8-dichloro-1-2-3-4-tetrahydroisoquinoline

1. The possible role of central beta-2 adrenoceptors and epinephrine pathways in opioid-induced prolactin (PRL) rise was investigated. 2. FK 33824, a synthetic opioid peptide injected into the third ventricle of Wistar male rats, generated a PRL rise that was significantly reduced by pretreatment with IPS 339, a potent and selective beta-2 antagonist. 3. Inhibition of central epinephrine synthesis with SKF 64 139, which selectively blocks phenylethanolamine-N-methyltransferase, partially decreased the PRL release induced by FK 33824. 4. Practolol, a selective beta-1 adrenoceptor blocker, did not modify the PRL secretion induced by FK 33824. 5. The results indicate that this FK 33824-induced PRL rise depends in part on the functional integrity of central beta-2 adrenoceptors and that epinephrine pathways in the brain may play an important role in the mechanisms by which opioid peptides increase PRL secretion.

Topics: Animals; D-Ala(2),MePhe(4),Met(0)-ol-enkephalin; Epinephrine; Isoquinolines; Male; Phenylethanolamine N-Methyltransferase; Prolactin; Propanolamines; Rats; Rats, Inbred Strains; Tetrahydroisoquinolines