INTRAVENOUS BETA-ENDORPHIN ADMINISTRATION FAILS TO ALTER HYPOTHALAMICBLOOD-FLOW IN RATS EXPRESSING NORMAL OR REDUCED NITRIC-OXIDE SYNTHASEACTIVITY

beta-Endorphin (beta-END) significantly contributes to the maintenance of hypothalamic blood flow (HBF) autoregulation during hemorrhagic hy potension in rats. Recently, several natural and synthetic opioid pept ides were reported to induce nitric oxide (NO)-mediated dilation in th e cerebrovascular bed. In the present study, the effect of beta-END wa s studied on HBF and hypothalamic vascular resistance (HVR) in vehicle -treated control rats and in rats after the pharmacological inhibition of the NO synthesis by chronic oral application of N-G-nitro-L-argini ne methyl ester. Intravenous beta-END administration failed to alter H BF or HVR either in control or in NO-blocked animals, and its transien t hypotensive effect was not inhibited by NO blockade, indicating that beta-END may not have NO-mediated vasodilator effect in the hypothala mic or in the systemic circulation.