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At least 109 records · Page 6Linked to original sources
PubMed1994

Intraventricular but not intraparaventricular nucleus metergoline elicits feeding in satiated rats.

Previous research has shown that systemic injections of the nonselective serotonin (5-HT) antagonist metergoline (MET) can stimulate feeding in both rats and humans. Five experiments were conducted to determine if this drug would elicit feeding in otherwise satiated rats after direct injections into the brain. In experiment 1, intraventricular infusions of 100 nmol MET produced reliable enhancements of feeding for 1 h compared with control infusions of a 5% tartaric acid (vehicle) solution. In experiment 2, a dose-response study of 0, 50, 100, and 150 nmol MET intraventricularly revealed that both 100 and 150 nmol doses reliably enhanced 1-h feeding, whereas 50 nmol did not. In experiment 3, tests of 90-min locomotor activity and water intake in the absence of food revealed that 100 nmol MET intraventricularly did not modify either behavior compared with vehicle infusions, suggesting a degree of feeding specificity to this effect. In an attempt to determine the site of intraventricular MET effects on feeding, experiment 4 tested 1-h feeding responses after 0, 5, 10, 20, 40, or 60 nmol MET were infused unilaterally into the paraventricular nucleus (PVN) of the hypothalamus. No reliable feeding was induced at any of these drug doses, although injections of 30 nmol norepinephrine (NE) were effective in doubling food intake. Experiment 5 further showed that bilateral infusions of 50 nmol MET in each PVN (total dose, 100 nmol) were ineffective in altering 1-h feeding. This contrasted markedly to the high potency of 15 nmol NE per site (total dose, 30 nmol), which elicited fivefold greater feeding than control infusions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

[Metergoline in hyperprolactinemic breast cancer: a phase II study].

The prolactin release inhibiting action of the dopamine receptor agonist metergoline was investigated in 16 patients with metastatic breast cancer associated with hyperprolactinemia. At a daily dose of 12 mg p.o. for 30 days, the drug was highly effective in lowering prolactin levels (day 0: 1076 +/- 171, day 29: 249 +/- 46 mU/l) in these patients. Starting treatment with 4 mg/day, the side effects of the treatment were mild, including dizziness and nausea.

Breast Neoplasms↗
PubMed1981

On the mode of the prolactin release-inhibiting action of the serotonin receptor blockers metergoline, methysergide, and cyproheptadine.

Using animals with large electrolytic lesions of the median eminence-mediobasal hypothalamus, we confirmed earlier findings that metergoline (ME) and methysergide (MS) inhibit PRL secretion through activation of the dopamine receptors of the pituitary lactotrophs and established, in a quantitative manner, that their dopaminergic potencies are comparable to the potency of the dopamine receptor agonist, piribedil, with ED50 in the order of 0.35 to 0.22 mg/kg. Cyproheptadine (CYP), acting by an unknown mechanism, had only a weak inhibiting effect (ED50 greater than 20.0 mg/kg) in these experimental conditions. In the second part of the study, the PRL-inhibiting actions of ME, MS, CYP, and piribedil, respectively, were tested against the PRL release-stimulating effect of activation of the central serotonergic system that was induced by administration of a large dose of L-5-hydroxytryptophan (5HTP; 100 mg/kg), a small dose of 5HTP (15 mg/kg) in rats pretreated with fluoxetine, or by the serotonin receptor agonist quipazine (10.0 mg/kg, ip). The inhibiting potencies of ME (ED50 0.019, 0.014, and 0.048 mg/kg, respectively) against these three stimuli were much larger than in the lesioned animals or than the corresponding potencies of piribedil (ED50 2.2, 0.24, and 0.41 mg/kg, respectively). It is assumed that in these experimental conditions ME inhibited PRL release by blockade of the central serotonin receptors in addition to its dopaminergic effect and that at low doses (0.1 mg/kg or less) the entire inhibiting effect of ME was probably due to its antiserotonergic activity. With MS, which is a weaker serotonin receptor blocker than ME (ED50 0.178, 0.075, and 0.55 mg/kg, respectively, for the three serotonergic stimuli of PRL release), the antiserotonergic component in its PRL-inhibiting effect was evident but less clearly separable from the dopaminergic component in experiments with 5HTP and with fluoxetine plus 5HTP, whereas in experiments with quipazine the entire action could be accounted for by its dopaminergic activity. CYP was the least potent among the three blockers (ED50 0.6, 0.4, and 1.37 mg/kg, respectively, for the three serotonergic stimuli of PRL release), but appropriate tests indicated that it acted only as a serotonin receptor blocker and not by virtue of its antihistaminic, anticholinergic properties or by a direct action on the pituitary lactotrophs. SQ 10,631, another serotonin receptor blocker that was also tested, had no PRL-inhibiting activity. Because of the dual nature of the PRL-inhibiting mechanism of ME and MS and the low effectiveness of CYP, combined possibly with other actions, the serotonin receptor blockers have limited value in studies concerning the role of the central serotonergic system in the regulation of PRL secretion.

Animals↗
PubMed1980

Anomalous growth hormone responses to thyrotropin-releasing hormone and glucose in cirrhotic patients: the effect of metergoline.

The anomalous GH response to TRH or glucose loading was evaluated in patients with severe liver disease untreated or pretreated with metergoline (MCE), a potent antiserotoninergic drug. In 9 patients, injection of 400 micrograms TRH as a bolus induced a clear-cut GH rise (> 8 ng/ml), with peak levels 15-90 min post injection. Pretreatment with MCE did not modify baseline GH levels but potentiated the TRH-induced GH rise in 4 patients. In addition, 2 of 8 TRH nonresponder patients developed the anomalous GH response after MCE pretreatment. Like MCE, methysergide, another antiserotoninergic drug, potentiated the TRH-induced GH rise in 2 of 4 patients. Glucose administration (100 g, orally) induced a paradoxical rise of GH in 9 of 10 patients; after MCE, the paradoxical GH response to glucose was potentiated in 6 patients. These data provide the first experimental evidence that a derangement in brain monoamine (serotonin) function is actually involved in the occurrence of anomalous GH responses in subjects with severe liver disease.

Ergolines↗
PubMed1991

[Use of metergoline in the treatment of infertility associated with hyperprolactinemia].

The usage of metergoline in patients with infertility and different forms (hinds) of hyperprolactinaemia was studied for 90 days at a dose of 12 mg. It gives a possibility to stimulate ovulation in 64% of patients and gain pregnancy in 8% of patients. In order to exceed the percentage of inpregnantion the course of medicine can be enlarged up to 6 months.

Female↗
PubMed1986

Monocrotaline pyrrole-induced cardiopulmonary toxicity is not altered by metergoline or ketanserin.

Monocrotaline pyrrole (MCTP) causes endothelial cell damage, pulmonary hypertension and right ventricular hypertrophy in rats by an undetermined mechanism. A role for 5-hydroxytryptamine (5-HT) in the cardiopulmonary response to MCTP has been suggested. To investigate the role of 5-HT, the effects of two 5-HT receptor antagonists were examined in MCTP-treated rats. Cotreatment with metergoline, an antagonist which binds to both 5-HT1 and 5-HT2 receptors, did not alter MCTP-induced elevation of lung weight or right ventricular hypertrophy. 5-HT-induced vascular smooth muscle contractions are mediated by 5-HT2 receptors; therefore, MCTP-treated rats were cotreated with ketanserin (KET), a specific 5-HT2 receptor antagonist. At a dosing regimen of KET that inhibited the 5-HT-induced platelet shape change in platelet-rich plasma and the 5-HT-induced increase in perfusion pressure in isolated lungs, KET did not affect the elevation in lung weight or the increased accumulation of 125I-albumin in the lung tissue of MCTP-treated rats. Moreover, MCTP-induced right ventricular hypertrophy was not attenuated by KET. These results indicate that cotreatment with either of these two 5-HT receptor antagonists does not alter the lung injury or right ventricular hypertrophic response to MCTP and suggest that 5-HT is not necessary for MCTP-induced toxicity.

Angiotensin II↗
PubMed1988

The interaction of metergoline, a 5-HT receptor blocker, and dexfenfluramine in human feeding.

Use of the 5-HT antagonist metergoline (MTG) has shown that dexfenfluramine (d-FF) influences food intake in animals via serotoninergic neurones. This study examined the interaction between d-FF and MTG in humans. Healthy male volunteers reported singly at 8:45 A.M. on four weekly occasions following an overnight fast. At 9:00 A.M. they received 30 mg d-FF or matching placebo and at 11:00 A.M. 4 mg MTG or placebo. Hunger and satiety were assessed hourly using visual analog scales (VAS). Subjects had access to a 4-channel automated food dispenser (AFD) from 1:15 to 3:15 P.M. Delivery and recording of each portion of known energy value was contingent on an appropriate button push. Subjects were offered two nonsweet snacks, plus fruit and a chocolate biscuit chosen to each subject's preference. Results for 13 subjects are reported. d-FF reduced hunger VAS, MTG had no effect on hunger and did not attenuate the effect of d-FF. d-FF reduced total food intake by 1306 kJ (312 kcal p less than 0.01) at 120 min. MTG increased food intake and attenuated the effect of d-FF on food intake but not significantly. d-FF markedly reduced the intake of nonsweet food; this was attenuated by MTG which alone had no effect on nonsweet food. d-FF had no effect on the intake of sweet tasting food during the first hour; by 120 min it had reduced energy intake by 342 kJ (82 kcal, t = 1.34, n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)

Drug Interactions↗
PubMed1982

Metabolism of metergoline in the rat.

[19,10-3H] Metergoline was administered orally to female rats and radioactive metabolites were recovered form urine and bile. Besides unchanged drug, the presence of 1-demethylmetergoline (II) was confirmed both in urine and bile. Two other urinary metabolites were identified, namely 8 beta-aminomethyl-6-methylergoline (IX) and 8 beta-acetylaminomethyl-6-methylergoline (VI). A third metabolite, 1,6-dimethyl-8 beta-aminomethylergoline (VIII), was identified only in bile. Beside these metabolites, further polar and so far unidentified biotransformation products are present both in bile and urine, accounting for about half of the radioactivity present in these excreta.

Administration, Oral↗
PubMed1977

Inhibition of prolactin release by metergoline administration in man.

Oral administration of metergoline, an antiserotoninergic agent, produced a fall in plasma prolactin concentrations in normal subjects. Prolactin values remained suppressed during a five day course of treatment with the drug. Serum growth hormone values were not altered significantly.

Adult↗