CENTRALLY ADMINISTERED NEUROPEPTIDE FF INHIBITS ARGININE-VASOPRESSIN RELEASE IN CONSCIOUS RATS

There is evidence indicating that neuropeptide FF (NPFF) is an endogen ous modulator of opioid systems. In the present study, we investigated the effect of centrally administered NPFF on arginine vasopressin (AW ) release in conscious rats. The plasma AVP increase in response to ei ther hyperosmolality rip injection of hypertonic saline (600 mosmol/kg )] or hypovolemia [ip injection of polyethylene glycol (PEG)I was sign ificantly blunted when NPFF was injected into the lateral ventricle so that the given drug could act at the hypothalamus and also reach the brain stem (hypertonic saline with 10 mu g/rat NPFF, 3.28 +/- 0.48 pg/ ml; hypertonic saline alone; 7.85 +/- 1.78 pg/ml; PEG with 10 mu g/rat NPFF, 4.07 +/- 1.40 pg/ml; PEG alone, 8.25 +/- 1.90 pg/ml). The plasm a AVP increase in response to PEG-induced hypovolemia was also attenua ted significantly and more potently when NPFF was injected into the ci sterna magna so that the given drug could be readily accessible to the dorsal medulla where the nucleus of solitary tract is located (10 mu g/rat; 2.71 +/- 0.14 pg/ml). In contrast, the NPFF injected into the c isterna magna had no significant effect on hyperosmolality-induced AVP release. Treatment with naloxone (10 mg/kg BW, sc) significantly reve rsed the inhibitory effects of NPFF on AVP release. These results sugg est that Central NPFF might play an inhibitory role via the hypothalam us in the osmoregulation of plasma AVP and via both the hypothalamus a nd the nucleus of solitary tract in the baroregulation, and that the i ntrinsic opioid systems are involved in the action of NPFF.