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There is evidence indicating that neuropeptide FF (NPFF) is an endogenous modulator of opioid systems. In the present study, we investigated the effect of centrally administered NPFF on arginine vasopressin (AVP) release in conscious rats. The plasma AVP increase in response to either hyperosmolality [i.p. injection of hypertonic saline (600 mosmol/kg)] or hypovolemia [i.p. injection of polyethylene glycol (PEG)] was significantly 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 micrograms/rat NPFF, 3.28 +/- 0.48 pg/ml; hypertonic saline alone, 7.85 +/- 1.78 pg/ml; PEG with 10 micrograms/rat NPFF, 4.07 +/- 1.40 pg/ml; PEG alone, 8.25 +/- 1.90 pg/ml). The plasma AVP increase in response to PEG-induced hypovolemia was also attenuated significantly and more potently when NPFF was injected into the cisterna magna so that the given drug could be readily accessible to the dorsal medulla where the nucleus of solitary tract is located (10 micrograms/rat; 2.71 +/- 0.14 pg/ml). In contrast, the NPFF injected into the cisterna magna had no significant effect on hyperosmolality-induced AVP release. Treatment with naloxone (10 mg/kg BW, sc) significantly reversed the inhibitory effects of NPFF on AVP release. These results suggest that central NPFF might play an inhibitory role via the hypothalamus in the osmoregulation of plasma AVP and via both the hypothalamus and the nucleus of solitary tract in the baroregulation, and that the intrinsic opioid systems are involved in the action of NPFF.

Centrally administered neuropeptide FF inhibits arginine vasopressin release in conscious rats.