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The effects of third ventricular (3V) injection of the @-adrenergic antagonist, propranolol (PROPR), a selective @,-antagonist, metoprolol (MET), a selective &-antagonist, IPS 339, and a @-adrenergic agonist (-) isoproterenol (ISOPR), on plasma concentrations of luteinking hormone (LH), follicle stimulating hormone (FSH), and growth hormone (GH) were studied in conscious, ovariectomized (OVX) rats. Samples were removed from unrestrained rats which had been previously implanted with atrial and 3V cannulae, and plasma hormone levels were determined by radioimmunoassay (RIA). Intraventricular injection of PROPR (30 pg), MET (40 pg), or IPS 339 (20 pg) induced a gradual elevation in plasma GH concentrations, whereas ISOPR (30 pg) reduced plasma GH. ISOPR (30 pg) brought about a decrease in plasma LH concentrations, but PROPR, MET and IPS 339 had no effect on LH levels. PROPR (30 pg) increased plasma FSH concentrations, but there was no significant effect of MET, IPS 339 or ISOPR on FSH secretion. The results indicate that the @-adrenergic system can inhibit the release of GH, LH, and FSH. This system appears to have a tonic inhibitory effect on GH and FSH but not LH release in the OVX rat.

The effects of third ventricular injection of naloxone and atropine, alone and together, on plasma concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL), growth hormone (GH), and thyroid-stimulating hormone (TSH) were studied in conscious, ovariectomized (OVX) rats. Samples were removed from unrestrained rats that had been previously implanted with an atrial cannula, and plasma hormone levels were determined by radioimmunoassay. Intraventricular injection of naloxone (30 micrograms) induced increases in plasma LH and GH concentrations, decreased plasma PRL levels, but did not alter plasma TSH. When atropine (100 micrograms) was injected intraventricularly, there was a decrease in plasma LH and an increase in PRL levels but no alterations in the levels of the other hormones. The action of naloxone on PRL and GH release was eliminated by simultaneous administration of atropine, but there was only a slight reduction in its effect on LH. The results indicate that central cholinergic neurons may play an important role, via muscarinic type receptors, in mediation of the effects of naloxone and presumably opiates on PRL and GH release, whereas the effects on LH appear to proceed independently of cholinergic neurons.