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At least 19 recordsLinked to original sources
PubMed1993

Comparison of induction of oestrus in dogs using metergoline, metergoline plus human chorionic gonadotrophin, or pregnant mares' serum gonadotrophin.

Twenty beagle bitches were treated with metergoline (groups I and II), ten with pregnant mares' serum gonadotrophin (PMSG; group III) and ten served as an untreated control group. Metergoline (12.5 mg per bitch) was injected intramuscularly (i.m.) every 3 days, starting between days 78 and 161 after the previous pro-oestrus. In 18 of the metergoline-treated bitches the interpro-oestrous interval (144 +/- 29 days) was significantly shorter (P < 0.01) than that of the control group (206.7 +/- 29.7 days). Of these 18 responder bitches, ten had not received human chorionic gonadotrophin (hCG) whereas eight had received 500 iu hCG i.m. in late pro-oestrus (group II). The durations of pro-oestrus and oestrus of the ten responding bitches not given hCG (6.8 +/- 5.5 and 11.7 +/- 4.5 days, respectively) did not differ (P > 0.05) from those of the control group (7.8 +/- 3.6 and 11.2 +/- 3.2 days). All ten bitches ovulated and nine became pregnant. Two of eight bitches responding to metergoline in group II exhibited a prolonged pro-oestrus after injection of hCG. In the remaining six bitches, the average duration of pro-oestrus and oestrus was 4.8 +/- 1.7 and 6.5 +/- 2.8 days, respectively, which was significantly shorter (P < 0.05) than in bitches not given hCG. The incidences of ovulation (6/8) and gestation (4/8) were lower than in bitches that received metergoline alone, or in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effect of metergoline on prolactin, follicle stimulating hormone, luteinizing hormone and thyroid stimulating hormone response to TRH and LHRH in normal men and women.

Metergoline, a prolactin (PRL)-lowering drug with an antiserotoninergic activity, is known to restore menstruations and fertility in hyper-PRL patients even when PRL levels are not normalized. This suggests that metergoline might also affect gonadotropins release. In a double-blind cross-over study in 8 normal males, repeated administration of metergoline enhanced the LH response to LHRH and reduced the PRL response to TRH; for females, three different tests were performed on days 5, 8 and 21 of two different menstrual cycles, each test being preceded by metergoline or by placebo administration. Metergoline always reduced the PRL response to TRH; on the 5th day, metergoline reduced the FSH response to LHRH and on the 21st day enhanced the LH response to LHRH. Basal levels of LH, FSH, T3, T4, Testosterone, 17 beta-estradiol and progesterone as well as the FSH response to LHRH (in males) and the TSH response to TRH (in both males and females) were not modified by metergoline. The data suggest that tests with TRH and LHRH can yield different results when performed during metergoline administration and that metergoline, acting through an unknown mechanism, can modify gonadotropins release.

Adult↗
PubMed1991

Metergoline blocks the behavioral and neuroendocrine effects of orally administered m-chlorophenylpiperazine in patients with obsessive-compulsive disorder.

The pharmacological probe, meta-chlorophenylpiperazine (m-CPP), administered orally to patients with obsessive-compulsive disorder (OCD) has been shown to induce an acute exacerbation in OCD symptoms as well as an exaggerated anxiogenic response in comparison with controls. The mechanism of m-CPP's behavioral effects in humans remains controversial. To further study m-CPP's actions in OCD patients, we completed a series of double-blind pharmacological challenges in 12 OCD patients. Six OCD patients received four separate challenges: placebo, metergoline, m-CPP, and metergoline plus m-CPP; the second group (n = 6) received metergoline and metergoline plus m-CPP in separate challenges. OCD patients receiving placebo or metergoline alone failed to show evidence of significant changes on any of the behavioral rating scales, in contrast to the patients who received m-CPP alone who exhibited significant increases in anxiety and OCD symptoms. However, the 12 OCD patients who received pretreatment with metergoline before m-CPP experienced no significant changes from baseline OCD symptoms or other behavioral changes. m-CPP's ability to elicit elevations in plasma prolactin was blocked by metergoline pretreatment. Metergoline's ability to block m-CPP's effects on behavior and plasma prolactin lends further support to a serotonergic mediation of m-CPP's effects, including its elicitation of OCD symptoms.

Administration, Oral↗
PubMed1983

[Suppression of puerperal lactation by metergoline].

Suppression of puerperal lactation by a potent serotonin antagonist, metergoline was studied in 33 puerperal women, i.e., abortion after sixteen weeks of gestation 6, premature labor 13, labor at term 13, and hydatiform mole 1. The drug was administered orally at a dose of 4 mg bid for 5 days to 26 subjects, starting within one week from delivery (group A). The remaining 7 subjects received 4 mg of metergoline bid for 7 days after more than 2 weeks from delivery (group B). Lactation was either rapidly suppressed or prevented in 22 out of the 26 subjects in group A and in all subjects in group B. After the therapy was stopped, rebound phenomena were observed in 4 subjects in group A and in 2 subjects in group B, but a further 5-7 days' treatment with metergoline produced satisfactory results. The mean plasma prolactin levels, studied in 10 subjects in group A at hourly intervals after the first metergoline dose, decreased significantly one hour later (p less than 0.05) and reached the nadir level, 19.9 +/- 2.6% of the mean basal value, 4 hours later. The daily plasma prolactin levels in 9 subjects were significantly lower than those of the control group during metergoline treatment (p less than 0.001). No side effects of metergoline medication were observed. Metergoline for a short course of administration is very effective in the suppression of puerperal lactation. In case of the suppression of lactation after the second week of puerperium, 10-14 days of metergoline treatment is recommended to avoid the rebound phenomena.

Adult↗
PubMedDate not supplied

[Puerperal inhibition of lactation with metergoline or bromocriptine].

In a controlled, randomised, prospective, clinical study, the effect of prolactin suppression and clinical course of the lactation suppressors Bromocriptine and Metergoline were investigated. During 7 months 150 patients were studied. 81 of those patients, who did not nurse, were treated by Bromocriptine (primary lactation suppression: n = 62, secondary suppression: n = 19) and 69 of the patients were treated by Metergoline (primary suppression: n = 54, secondary suppression: n = 15). The drugs were administrated orally to all subjects, dosed 2 x 2.5 mg/d of Bromocriptine for 14 days and 3 x 4 mg/d of Metergoline for 10 days, starting in average after 13 hours. Puerperal suppression of prolactine were compared with randomised breast feeding subjects (n = 30). In Bromocriptine treated women the average plasma prolactin level decreased from 78.4 +/- 22 ng/ml to 17.0 +/- 3.3 ng/ml during five days of treatment. In Metergoline treated women the plasma prolactin level decreased from 129.7 +/- 15.1 ng/ml to 56.9 +/- 10.0 ng/ml during the first days of treatment. Prolactin level of breast feeding subjects decreased from 233.6 +/- 21.4 ng/ml to 185.8 +/- 23.7 ng/ml during the same period (p < 0.05). There is no statistical significancy of clinical difference of both drugs, but a statistical trend was seen. With Bromocriptine treated women were suppressed efficiently in 71 of 81 cases, 10 refused. Refusals were divided in two quality levels, level I with subjects with moderate complaints and little puerperal lactation, level II with subjects with considerable complaints including strong puerperal lactation. With Metergoline suppressed women, treatment was efficiently in 51 of 69 cases, but refusals of level I were observed in 11 cases and refusals of level II were observed in 7 cases. The results show that Bromocriptine and Metergoline are effective on suppression of lactation. Under the current drug dose of Metergoline an advantage of Bromocriptine were observed. Only further studies could investigate, whether an adaptation of drug dose would improve the clinical efficiency of Metergoline.

Administration, Oral↗
PubMed1977

Stimulating action of sulpiride and pimozide on prolactin release. Effect on bromocriptine, L-dopa and metergoline administration.

In order to evaluate the mechanism of action of metergoline, an antiserotonin agent, the effect of pre-treatment with metergoline on prolactin (PRL) release induced by sulpiride was compared to that obtained after bromocriptine administration in normal subjects. In addition, the metergoline effect on PRL release induced by pimozide, specific dopamine receptor blocking agent, was compared to that obtained with L-dopa. Metergoline administration resulted in definite decrease in plasma PRL in all subjects; however, metergoline did not block, differently from bromocriptine, the PRL release induced by sulpiride. On the contrary, metergoline, like L-dopa, inhibited PRL release induced by pimozide pre-treatment. These results raise the possibility that metergoline does not act as an antiserotonin agent; its antilactogenic effect observed under basal conditions may be dependent on different mechanisms of action.

Adolescent↗
PubMed1978

Paradoxical decrease of brain 5-HT turnover by metergoline, a central 5-HT receptor blocker.

Since metergoline (1-methyl-8-beta-carbobenzyloxy-aminomethyl-10-alpha-ergoline) is a potent 5-HT antagonist in peripheral organs, its possible blocking effects on 5-HT receptors in the rat brain were investigated. In vitro, metergoline inhibited both the specific high affinity binding of 3-H-5-HT onto synaptosomal membranes (IC 50 = 18 nM) and the stimulating effect of 10 micron 5-HT on the adenylate cyclase activity in colliculi homogenates from newborn rats (IC 50 = 12 micron. In vivo, the administration of metergoline (10 mg/kg i.p., 60 min before death) resulted in a significant decrease in the 3-H-5-HT binding capacity of synaptosomal membranes from the forebrain of adult rats. Taken together, these data clearly indicated that metergoline is a potent blocker of some serotoninergic receptors in the rat brain. Surprisingly, the changes in 5-HT turnover occurring in the brainstem and in the forebrain 1 h after metergoline (2-10 mg/kg) treatment were similar to those normally induced by a central 5-HT agonist: both the rate of 5-HT utilisation and that of 5-HT synthesis were significantly decreased. These changes were in contrast to the acceleration of 5-HT turnover induced by the administration of another potent central 5-HT antagonist, methiothepin. These results are discussed in relation to the possible existence of several types of serotoninergic receptors in the rat brain. It is possible that the positive feedback regulation of 5-HT turnover is triggered by the blockade of serotoninergic receptors sensitive to methiothepin, but not to metergoline.

Adenylyl Cyclases↗
PubMed1983

Effect of metergoline on the aldosterone-stimulating properties of metoclopramide.

The mechanism by which metoclopramide stimulates aldosterone secretion is still unclear, since it cannot be explained by known regulatory systems. On the other hand we have recently shown that serotonin is also a potent aldosterone-stimulatory substance in man and its action can be blunted by the antiserotoninergic drug, metergoline. To test if metoclopramide could act through a serotoninergic pathway we have studied the effect of metergoline on the aldosterone response to metoclopramide in 8 normal subjects. The effect of metoclopramide (10 mg i.v.) on plasma aldosterone, PRA, cortisol, prolactin and K was studied before and after acute metergoline administration. Metergoline pretreatment significantly reduced the aldosterone response to metoclopramide, together with a slight reduction of prolactin, whereas no changes were seen on PRA, cortisol and K. In vitro, metoclopramide induced a significant aldosterone output from human adrenal adenoma cells, which was partially reduced by metergoline and not by bromocriptine. Despite a lack of specificity of metergoline these data may suggest the hypothesis of a serotoninergic component in the aldosterone-stimulating properties of metoclopramide.

Adenoma↗
PubMed1981

[3H]Metergoline: a new ligand of serotonin receptors in the rat brain.

A specific binding site for [3H]metergoline characterized by a KD of 0.5-1.0 nM was detected in microsomal and synaptic plasma membranes from various areas of the adult rat brain. Experiments with 5,7-dihydroxytryptamine- and kainic acid-induced lesions indicated that this specific binding site was localized post-synaptically with respect to serotoninergic neurons. The pharmacological characteristics of [3H]metergoline binding to microsomal membranes from the whole forebrain strongly suggest that this ligand labels a class of serotonin receptors. This was particularly obvious in the hippocampus in which serotonin was about 400 times more potent than dopamine and noradrenaline for displacing bound [3H]metergoline. In the striatum, serotonin was only 10 times as potent as dopamine in inhibiting [3H]metergoline binding, suggesting that this ligand may also bind to dopamine receptors. Striking similarities between the binding sites for [3H]metergoline and [3H]serotonin were observed in the hippocampus. Thus, not only the total numbers of binding sites for these two ligands in control rats but also their respective increases following intracerebral 5,7-dihydroxytryptamine treatment were very similar. Therefore, at least in the hippocampus, [3H]metergoline might well be the appropriate ligand for studying the characteristics of the 'antagonist form' of serotonin receptors postulated by Bennett and Snyder.

5,7-Dihydroxytryptamine↗
PubMed1979

The effects of metergoline and other serotonin receptor antagonists on serum corticosterone in rats.

Metergoline antagonized the elevation of serum corticosterone by quipazine in rats. The ED50 of metergoline was less than 0.1 mg/kg, ip, and the effects of a 3 mg/kg dose persisted for more than 24 h. Metergoline did not antagonize the elevation of serum corticosterone by theophylline or ketamine (i.e. did not prevent corticosterone release nonspecifically) and did not affect the concentration of quipazine in the brain. Since quipazine is a serotonin receptor agonist, the antagonistic effects of metergoline may have been due to competition with quipazine at serotonin receptor sites in the brain. Some other agents capable of blocking serotonin receptors also antagonzied the elevation of serum corticosterone by quipazine. These included LY53857, which gave complete blockade at 3 mg/kg, and cyproheptadine and spiperone, which gave significant but incomplete antagonism at 1 mg/kg. Methysergide at 3 mg/kg did not alter the effect of quipazine. Metergoline did not antagonize the elevation of serum corticosterone by other agents throught to act via serotoninergic mechanisms, namely fluoxetine, fenfluramine, L-5-hydroxytryptophan, N,N-demthyl-5-methoxytryptamine, and 1-(m-trifluoromethylphenyl)piperazine. Thus, the interactions between metergoline and quipazine may have occurred at receptors that are not serotonin receptors or that represent a subset of serotonin receptors not mediating the actions of serotoninergic agents other than quipazine.

Animals↗
PubMed1981

Behavioural effects of long term inhibition of 5-hydroxytryptamine receptors using metergoline.

1. Rats were treated with acute and chronic schedules of metergoline (2.5 mg/kg I.P. twice daily) and acutely with dl-propranolol (15 mg/kg), amitriptyline (12.5 mg/kg) and fluoxetine (2 mg/kg). 2. Metergoline given both acutely and chronically blocked the behavioural response to the 5-hydroxytryptamine receptor agonist 5-methoxy-N1, N1-dimethyltryptamine (5MeODMT) (2.5 mg/kg I.P.). The response to 5MeODMT) was also blocked by acute administration of dl-propranolol and amitriptyline, but not fluoxetine. 3. Rats given chronic treatment with metergoline and then withdrawn from drug treatment for 3 days showed an enhanced response to 5MeODMT. 4. Chronic metergoline treatment caused an increase in ambulatory movement following 5MeODMT administration. 5. Exploratory behaviour, when measured under dark conditions, was reduced by chronic metergoline treatment. 6. The results suggest that supersensitivity to 5-hydroxytryptamine agonists can be induced by chronic treatment with an antagonist. Furthermore, metergoline and 5-methoxy-N1, N1-dimethyltryptamine may not act on identical receptor populations.

Amitriptyline↗
PubMed1987

Development of tolerance to the antinociceptive effect of metergoline.

Metergoline given IP reduced the response to noxious stimulation in the mouse formalin test. Tolerance to this effect developed after a chronic treatment schedule consisting of ten daily injections of 5 mg/kg. Twenty four hours after the last injection a test dose of metergoline (2.5 mg/kg) reduced the licking time in the formalin test by 28% in the chronic metergoline group, compared to 68% reduction in the vehicle-treated animals. In addition, the antinociceptive effect of the 5-hydroxytryptamine releasing compound p-chloramphetamine (PCA) was reduced following chronic treatment with metergoline. The reduced effect of PCA may have been caused by down-regulation of 5-HT2 receptors. However, this finding is also compatible with the contention that metergoline may act as an agonist at postsynaptic serotonergic receptors.

Animals↗
PubMed1986

Failure of pimozide and metergoline to antagonize the RDS-127-induced facilitation of ejaculatory behavior.

Metergoline, a serotonin-receptor antagonist, when administered in either an ascorbic acid or ethanol containing vehicle was without effect on male rat copulatory behavior (3 mg/kg, 90 minutes pretest). When initially dissolved in several drops of acetic acid, however, the same dose of metergoline dramatically suppressed male rat sexual behavior. Thus, one-half of the treated rats failed to intromit and ejaculate, and those displaying the behaviors exhibited elongated intercopulatory and postejaculatory intervals. The administration of the putative dopamine-receptor agonist RDS-127 (2-N,N-di-n-propylamino-4,7-dimethoxyindane; 3 mg/kg, six minutes pretest) induced seminal emission ex copula and drastically reduced intromission frequency and ejaculation latency in copula, as well as effecting lesser reductions in the intercopulatory and postejaculatory intervals in two sequential copulatory series. RDS-127-induced seminal emission was effectively antagonized by pretreatment with the dopamine-receptor antagonist pimozide (250 micrograms/kg, two hours pretest), but not by pretreatment with metergoline. In contrast to seminal emission ex copula, pimozide pretreatment failed to antagonize the RDS-127 facilitation of ejaculatory behavior in copula. Metergoline pretreatment also failed to antagonize the RDS-127-induced facilitation of ejaculatory behavior in copula. However, RDS-127 prevented the suppressive effects of metergoline treatment, suggesting that RDS-127 has some agonistic action at serotonergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Increased self-administration of d-amphetamine by rats pretreated with metergoline.

Rats trained to self-administer d-amphetamine were pretreated with metergoline, a long-acting 5-hydroxytryptaminergic antagonist, and immediately placed in self-administration cages for 8 hours. During the first 3 hours after metergoline the normal pattern of d-amphetamine self-administration was unaltered, but thereafter the rate of self-injections was increased. Between 4 and 6 hr the self-injections in metergoline-treated rats were increased in a regular fashion and subsequently (7-8 hr) in a stereotyped manner, i.e., rapid bursts of lever presses with little space between injections. In amphetamine-naive rats the levels of striatal and nucleus accumbens dopamine metabolites, dihydroxyphenylacetic acid and homovanillic acid, rose with time after metergoline injection. Levels of 5-hydroxyindoleacetic acid remained unchanged in these brain areas. The neurochemical results suggest a correlation between the dopaminergic actions of metergoline and d-amphetamine self-administration.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

Antagonism of metergoline on the diuretic effect of cyclazocine and U-50488 drugs with a kappa agonist activity.

In rats receiving a normal saline load of 2.5 ml/100 g, sc, (moderately hydrated rats), injections of the serotonin (5-HT) antagonist, metergoline (0.25-1-4 mg/kg), resulted in a dose-dependent decrease in the urine output induced by a dose of 8 mg/kg of cyclazocine (a benzomorphan derivative, mixed kappa and sigma agonist) at the 2-h time period. The antagonist effect of metergoline (1 mg/kg) on cyclazocine doses ranging from 0.25 to 8 mg/kg, was observed only at 2 mg/kg higher doses. Other 5-HT receptor blockers, methysergide, pizotifen, cyproheptadine, caused a significant degree of antagonism. In rats receiving a saline load and a water load of 5.5 ml/100 g, ip (hyperhydrated rats), metergoline (1 mg/kg) completely antagonized the diuretic effect of cyclazocine (8 mg/kg) at the 4-h and 5-h time periods. Similarly, metergoline (1 and 4 mg/kg) administered in moderately hydrated rats, markedly decreased at the 2-h time period, the urine output produced by 5 mg/kg of U-50488 (a non benzomorphan derivative, highly selective kappa agonist), and in hyperhydrated rats, completely suppressed, at the 4-h and 5-h time periods the drug-induced diuresis. Metergoline administered alone had no effect on urine output in moderately hydrated rats or in hyperhydrated rats. These results suggest the hypothesis that 5-HT may be involved in the complex mechanisms of kappa agonist-induced diuresis in rats.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1991

The behavioural response to intrathecal serotonin is changed by acute but not by repeated treatment with zimelidine or metergoline.

The behavioural response to intrathecal serotonin (5-HT) was examined in mice after acute and after withdrawal of repeated treatment with the 5-HT uptake inhibitor zimelidine or the 5-HT receptor antagonist metergoline. Intrathecal 5-HT elicits a response consisting of biting or licking of the lower part of abdomen and reciprocal hindlimb scratching, indicative of nociceptive stimulation. Acute injection of zimelidine (20 mg/kg) significantly increased the response to intrathecal 5-HT (0.25-1 micrograms) whereas a single dose of metergoline (5 mg/kg) completely blocked the response to intrathecal 5-HT (2 micrograms). The behavioural response to intrathecal 5-HT (0.25-2 micrograms) was not significantly changed 48 hr after withdrawal of repeated treatment with zimelidine (2 x 10 mg/kg/day for 14 days) or metergoline (2 x 2.5 mg/kg/day for 14 days). In the present experiments acute zimelidine appeared to increase nociceptive responsiveness, whereas metergoline had the opposite effect. This study does not provide evidence that long-term treatment with zimelidine or metergoline leads to adaptive changes in the response to spinal cord 5-HT receptor stimulation.

Animals↗
PubMed1977

Metergoline in the inhibition of puerperal lactation.

Seventy-eight mothers who did not want to breast-feed their newborn infants took part in a trial to assess whether metergoline could effectively suppress puerperal lactation. Metergoline 8 mg/day was given to 69 women within 24 hours after delivery and continued for five days to prevent lactation. The remaining nine women were given a course of metergoline once lactation had started. The drug was effective in both preventing and suppressing lactation. Milk secretion, engorgement, and pain were significantly reduced in women taking metergoline. Metergoline has a similar effect to bromocriptine in suppressing lactation, but its mechanism of action remains unknown.

Clinical Trials as Topic↗
PubMed1983

Inhibition of puerperal lactation by metergoline: interactions with methylergobasine maleate.

Metergoline, a prolactin (PRL) lowering drug, is used in the puerperal period to inhibit lactation. Methylergobasine maleate (MEM), widely employed in the puerperium to promote uterine contractions, has also been reported to decrease PRL release and to reduce lactation. To evaluate the possible interactions of the two drugs, groups of 6-11 puerperae each received no treatment, metergoline alone (8 or 12 mg/day for 5 days), MEM alone (0.2 mg i.v. at delivery followed by 0.5 mg/day p.o. for 5 days) and metergoline plus MEM. Metergoline fully prevented lactation and significantly reduced PRL release, the higher dose inducing effects faster. MEM was without effect on PRL release and lactation, and did not modify the effect of metergoline.

Adolescent↗