EFFECTS OF PITUITARY BETA-ENDORPHIN SECRETAGOGUES ON THE CONCENTRATION OF BETA-ENDORPHIN IN RAT CEREBROSPINAL-FLUID - EVIDENCE FOR A ROLE OF VASOPRESSIN IN THE REGULATION OF BRAIN BETA-ENDORPHIN RELEASE

The concentration of P-endorphin-immunoreactivity (bE-IR) in cerebrospinal fluid (CSF) and plasma of rats was determined following intracerebroventricular (ICV) treatment of conscious animals with substances known to stimulate the release of PE and other pro-opiomelanocortin (POMC)-derived peptides at the level of the anteriorand intermediate lobes of the pituitary. The p-adrenoceptor agoinst isoproterenol (ISO) did not influence the concentration of PE-IR in CSF collected 5-60 min after ICV administration of doses ranging from 3 to 30,000 pg/rat. Plasma bE-IR levels, however, were significantly increased 20 min following ICV injection of 30,000 pg ISO. ICV treatment of animals with ovine corticotropin-releasing factor (CRF; 30-30,000 pg/rat) also did not affect CSF levels of bE-IR, whereas CRF in a dose of 30 pg significantly decreased, and in doses of 300-30,000 pg enhanced plasma bFE-IR concentrations as determined by 20 min following treatments. ICV injection of arginine8-vasopressin (AVP) in doses of 10-1,000 pg/rat dose-dependently elevated the bE-IR concentration in CSF without affecting plasma bE-IR levels. This AVP-induced increase in CSF PE-IR was maximal 20-35 min and bE-IR levels had returned to basal 60 min following treatment. The data indicate that AVP and not ISO and CRF is a stimulator of CSF levels of bE-IR. As bE-IR in CSF likely originates from brain POMC neurons, these results suggest the hot vasopressin may be a physiological regulator of brain POMC activity, and may act as a releasing factor for POMC-derived peptides in the brain. © 1990 S. Karger AG, Basel.