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PubMed1987

Pulsatile luteinizing hormone secretion and clomiphene and bromocriptine response in amenorrheic women with normoprolactinemia and gestagen withdrawal bleeding.

This study was carried out to determine whether the ovulatory response with clomiphene citrate and bromocriptine in 20 amenorrheic women with normoprolactinemia and gestagen withdrawal bleeding is influenced by the pretreatment pattern of pulsatile luteinizing hormone (LH) secretion. Two patients who had no LH pulse for 3-5 h failed to respond to clomiphene. One of them was treated with bromocriptine, but ovulation did not occur. Eleven of 12 patients who had one or more LH pulses and LH pulse/h ratios of less than 1 for 3-5 h ovulated with clomiphene. One clomiphene nonresponsive patient ovulated with combined therapy of bromocriptine and clomiphene. All 6 patients who had LH pulse/h ratios of greater than or equal to 1 for 3-5 h failed to ovulate with clomiphene. Three of them were treated with bromocriptine. Two of 3 patients ovulated with bromocriptine alone and 1 ovulated with combined therapy of bromocriptine and clomiphene. These results suggest that the pretreatment pattern of pulsatile LH secretion may predict the clinical response to clomiphene and bromocriptine treatment in amenorrheic women with normoprolactinemia and gestagen withdrawal bleeding.

Adult↗
PubMed1992

Bromocriptine inhibits pro-opiomelanocortin mRNA and ACTH precursor secretion in small cell lung cancer cell lines.

We have previously reported that a human small cell lung cancer (SCLC) cell line (COR L103) that expresses the proopiomelanocortin (POMC) gene and secretes ACTH precursor peptides is relatively resistant to glucocorticoid regulation. Using this model, we have now examined alternative regulatory mechanisms of the POMC gene and found that both the mRNA and ACTH precursor peptides were stimulated four- and two-fold, respectively, after 48 h incubation with db-cAMP. Next, we examined the dopamine agonist, bromocriptine, which acts predominantly through D2 receptors linked to adenyl cyclase to cause a reduction in intracellular cAMP. Bromocriptine suppressed cAMP levels and inhibited precursor peptide secretion within 24 h in a dose-dependent manner (0.15-15 microM). At the highest dose, peptide secretion was inhibited from 95 to 53 pmol/mg protein, and POMC mRNA was reduced by 50%, while beta-actin mRNA remained unchanged. This effect could not be mimicked by incubation of cells with the alpha-adrenergic antagonist, phenoxybenzamine, suggesting that the alpha-adrenergic effects of bromocriptine were not responsible for this observation. These cells also secrete estradiol, but the secretory rate was unaffected by bromocriptine, suggesting, with the beta-actin data, that the POMC inhibition was not a cytotoxic effect. No recovery in precursor peptide secretion was seen in a 48-h period after the removal of bromocriptine. However, when the postchallenge incubation was extended to 8 d, there was a recovery in secretory potential between day 3 and day 8 and normal growth kinetics in the 4 d after removal of the drug. In contrast to these findings, the mouse corticotroph cell line, AtT20, showed no response to bromocriptine, in keeping with reports that this agonist has no effect on anterior lobe corticotrophs. We conclude that bromocriptine effectively inhibits POMC expression in SCLC cells, and that this phenomenon might be of useful clinical application.

Adrenocorticotropic Hormone↗
PubMed1999

Effects of bromocriptine and haloperidol on prepulse inhibition: comparison of the acoustic startle eyeblink response and the N1/P2 auditory-evoked response in man.

Experiments with animals have shown that D2 dopamine receptors are involved in regulating prepulse inhibition (PPI) of the acoustic startle reflex (suppression of the reflex response evoked by a loud sound by prior presentation of a low-intensity stimulus). Recently we found that PPI of the human eyeblink startle response could be suppressed by a D2 receptor agonist, bromocriptine, and that this suppression could be reversed by a D2 receptor-blocking neuroleptic, haloperidol. The present work attempted to replicate this finding and to extend it to PPI of the N1/P2 component of the auditory-evoked potential. Eleven healthy males (18-30 years) participated in four sessions in which they received oral doses of placebo, bromocriptine 1.25 mg, haloperidol 3mg and combined treatment with bromocriptine 1.25 mg + haloperidol 3 mg, according to a balanced double-blind protocol. Thirty-minute simultaneous recordings of the electromyographic (EMG) responses of the orbicularis oculi muscle of the right eye and the vertex auditory-evoked potentials took place 120 min after ingestion of haloperidol and/or 90 min after ingestion of bromocriptine. Sound stimuli (1-kHz) were presented in 60 trials separated by variable intervals (mean 25 sec): (i) 40 msec 115 dB ('pulse alone': 20 trials); (ii) 40 msec 85 dB (20 trials); (iii) 40 msec 85 dB, followed after 120 msec by 40 msec 115 dB ('prepulse/ pulse': 20 trials). The amplitudes of the EMG and N1/P2 responses were not altered significantly by any of the treatments. Bromocriptine attenuated PPI of the EMG response significantly, this attenuation being absent following combined haloperidol/bromocriptine treatment. Neither bromocriptine nor haloperidol significantly altered PPI of the N1/P2 complex. Bromocriptine suppressed and haloperidol elevated serum prolactin levels, these changes being absent when the two drugs were given in combination. The results suggest that different mechanisms may be involved in regulating PPI of the eyeblink and the N1/P2 component of the auditory-evoked potential, and that D2 receptors may be involved in the former case, but not the latter.

Acoustic Stimulation↗
PubMed1997

Pleural disease during treatment with bromocriptine in patients previously exposed to asbestos.

Bromocriptine, which is used in the treatment of Parkinson's disease, can cause adverse pleuropulmonary reactions. Exposure to asbestos can result in similar lesions. Fifteen patients with former exposure to asbestos, who developed pleural fibrosis after treatment with bromocriptine, were observed independently in Sweden (11 patients) and Australia (four patients). The patients complained of malaise, often associated with weight loss, dyspnoea, and a disturbing cough. Laboratory values included increased erythrocyte sedimentation rate and a low haemoglobin level. Lung function tests showed a restrictive lung function defect. Chest radiographs showed bilateral pleural fibrosis, with small amounts of fluid in some cases. Soon after bromocriptine was withdrawn, the patients improved clinically, and the laboratory values returned to normal. However, in most cases, pleural fibrosis and a restrictive lung function defect persisted to some extent. In conclusion, in patients who develop pleuropulmonary fibrosis whilst being treated with bromocriptine, former exposure to asbestos should be investigated. Conversely, when pleural changes develop in a patient on bromocriptine and with prior exposure to asbestos, the possible causative role of the drug should be discussed. Special follow-up may be indicated when bromocriptine is planned in a patient with previous asbestos exposure, and if symptoms or signs of pleural fibrosis develop, bromocriptine withdrawal should be considered.

Adolescent↗
PubMed2001

Bromocriptine treatment of systemic lupus erythematosus.

Prolactin, a peptide hormone, acts as a cytokine. It has been hypothesized that bromocriptine, a dopamine analog that suppresses pituitary secretion of prolactin, suppresses circulating prolactin and, through this mechanism, has the potential to suppress autoimmune disease. This rationale has been applied to the treatment of systemic lupus erythematosus (SLE), a prototype autoimmune illness that occurs spontaneously in animal models such as the F1 hybrid NZBxNZW mouse, and in humans. Treatment with bromocriptine was effective in treating some induced and spontaneous autoimmune disease in experimental models. Bromocriptine did slow the course of SLE in NZBxNZW mice when treatment was started before the appearance of clinical disease. In addition, bromocriptine was effective in treating established disease in this model. In three separate clinical trials, bromocriptine showed evidence that it had a therapeutic effect in treating human lupus. Bromocriptine is currently considered an unproven therapy for SLE. Its use is entirely experimental. The fact that bromocriptine was effective in treating NZBxNZW mice, the beneficial therapeutic effects in human trials, and the low toxicity of the drug form a solid rationale for undertaking further therapeutic trials.

Animals↗
PubMed1976

Prolactin and thyrotropin responses to thyrotropin-releasing hormone in patients with secondary amenorrhea: the effect of bromocriptine.

Prolactin (PRL) and thyrotropin (TSH) responses to a 200 mug intravenous thyrotropin-releasing hormone (TRH) bolus were measured by radioimmunoassay in 11 women with hyperprolactinemic amenorrhea and 9 with normoprolactinemic amenorrhea. In all cases, the tests were carried out under basal conditions and repeated during bromocriptine treatment. In women whose basal PRL level was normal; TRH caused a maximal PRL increment of 85 +/- 25.2 mug/l (mean +/- SE), while those women whose basal PRL level was raised showed a smaller increase (5.2 +/- 11.9 mug/l) (P=0.02). The peak levels were not significantly different in these two groups (95.0 +/- 26.7 and 134.6 +/- 35.9 mug/l) (P is greater than 0.1). During bromocriptine treatment, the raised PRL levels decreased in all cases, but levels over 30 mug/l remained in 3 patients, one of whom turned out to have a pituitary tumor. Prolactin responses to TRH were markedly inhibited in normoprolactinemic patients by the dose of bromocriptine used. The mean maximal net increase of PRL was 2.0 +/- 0.9 mug/l in normoprolactinemic patients and 11.0 +/- 8.1 mug/l in hyperprolactinemic patients taking bromocriptine. After TRH stimulation during bromocriptine, the peak PRL levels in hyperprolactinemic patients were higher (32.7 +/- 10.5 mug/l) than in normoprolactinemic patients (7.2 +/- 1.5 mug/l). Unlike what has been described for hypothyroid patients, the basal TSH level in euthyroid amenorrhea patients was not affected by bromocriptine, and we found that bromocriptine has no effect on the TRH-TSH response.

Adult↗
PubMed1979

Bromocriptine in Parkinson disease: further studies.

Bromocriptine was administered to 66 patients with advanced Parkinson disease (PD) and increasing disability despite optimal treatment with levodopa/carbidopa (Sinemet). Forty-five patients tolerated at least 25 mg per day of bromocriptine (the "adequately treated" group) in addition to Sinemet and had significantly decreased rigidity, tremor, bradykinesia, gait disturbance, and total score, but increased involuntary movements. Twenty-five of these 45 patients improved by at least one stage. Among the 45 patients, 27 had "on-off" effects, and in 19 the "on-off" effects decreased on bromocriptine. The mean dose of bromocriptine in adequately treated patients las 47 mg, permitting a 10 percent reduction in the dose of levodopa. Twelve adequately treated patients received bromocriptine for at least 1 year, and 8 continued for longer than this. Bromocriptine was discontinued in 29 of 66 patients because of adverse effects, including mental changes (14 patients) and involuntary movements (9 patients). All adverse effects were reversible. Despite adverse effects, expense, and scarcity, bromocriptine, when added to levodopa, is useful in patients with advanced disease who no longer respond satisfactorily to levodopa, and for whom no other treatment is available.

Adult↗
PubMed1999

A 3-year randomized trial of ropinirole and bromocriptine in early Parkinson's disease. The 053 Study Group.

OBJECTIVE: To compare the long-term efficacy and safety of ropinirole with bromocriptine over 3 years in patients with early PD with limited or no previous dopaminergic therapy. METHODS: In this prospective, double-blind, parallel-group study, 335 patients were randomized to 0.75 mg ropinirole or 1.25 mg bromocriptine titrated upward at weekly intervals--maximum permitted daily doses were 24 mg ropinirole, 40 mg bromocriptine. RESULTS: Approximately one third of patients in each group withdrew prematurely, mostly because of adverse experiences; 61/102 (60%) of ropinirole-treated and 59/112 (53%) of bromocriptine-treated patients completed the study on the dopamine agonist alone. Mean doses for all patients at completion were 12 mg (SD 6) ropinirole and 24 mg (SD 8) bromocriptine. Occurrence of adverse experiences in both groups was similar. Emergence of dyskinesias was low. Both treatments induced marked improvements in Unified Parkinson's Disease Rating Scale activities of daily living (ADL, Part II) and motor (Part III) scores over the first 12 weeks, which were maintained during the study. After 3 years, patients in the ropinirole group had a mean improvement in motor score of 31% compared with 22% in the bromocriptine group (p = 0.086) and a significantly better ADL score (treatment difference 1.46 points, p = 0.009) [corrected]. CONCLUSIONS: Both dopamine agonists are effective in the early treatment of a high proportion of PD patients; effectiveness persists for at least 3 years. Those who completed the study had a significantly better functional status on ropinirole than on bromocriptine.

Activities of Daily Living↗
PubMed1993

Terguride as a new anti-hyperprolactinemic agent: characterization in rats and dogs in comparison with bromocriptine.

Terguride, a derivative of the ergot alkaloid, was characterized as a new anti-hyperprolactinemic agent in rats and dogs in comparison with bromocriptine. Terguride was found to bind selectively to the pituitary dopamine D2-receptors with a high affinity (Kd = 0.39 nM). In reserpinized rats, terguride at 0.03 mg/kg, p.o. significantly reduced the serum prolactin (PRL) level. The PRL lowering effect and the effective dose were longer lasting and about 30 times lower than those of bromocriptine, respectively. In rats bearing estrogen-induced pituitary prolactinoma, chronic terguride induced shrinkage of the prolactinoma as well as reduction of the high serum PRL level. In lactating rats, terguride (1.0 mg/kg, s.c.) reduced milk production in the mammary gland, whereas bromocriptine showed no significant effect up to 10 mg/kg, s.c. Terguride (10 mg/kg, p.o.) did not induce any stereotypy and hypermotility in reserpinized rats, while bromocriptine induced both stereotypy and hypermotility significantly at 10 mg/kg, p.o. In dogs, terguride, like bromocriptine, reduced the serum PRL level, but did not affect the serum levels of growth hormone and luteinizing hormone. In dogs, bromocriptine induced both emesis and PRL-lowering at almost the same dose, whereas emesis-inducing doses of terguride were about 100 times higher than the PRL-lowering dose. These results suggest that terguride as a dopamine D2-agonist is a potent inhibitor of PRL secretion with less neurotropic side effects compared to bromocriptine, and thus a useful drug for the treatment of galactorrhea and hyperprolactinemia including prolactinoma.

Animals↗
PubMed2004

Acute onset of severe dilated cardiomyopathy during bromocriptine therapy.

OBJECTIVE: To report a case of severe dilated cardiomyopathy (DCMP) in a patient on bromocriptine therapy for a microprolactinoma. CASE SUMMARY: A 31-year-old African American female, who had been receiving bromocriptine 5 mg orally daily for a microprolactinoma during the preceding month, developed severe DCMP. An echocardiogram showed a markedly dilated left ventricle with severe reduction in the left-ventricular ejection fraction in the absence of any other identifiable causes of DCMP such as a peripartum state, ethanol use, preceding systemic viral illness, chronic hypocalcemia, chronic hypophosphatemia, or chronic uncontrolled tachycardia. She improved substantially (both symptomatically and echocardiographically) after cessation of bromocriptine therapy and initiation of supportive treatment of congestive heart failure (CHF). She showed no recurrence of CHF at a follow-up visit 2 months after withdrawal of the supportive care. The patient was not rechallenged with bromocriptine due to the clinical/ethical gravity of this probable adverse effect. DISCUSSION: Although cardiopulmonary adverse effects have been reported with the use of cabergoline (another dopamine agonist), to the best of our knowledge, this is the first case report of severe life-threatening DCMP associated with bromocriptine therapy. Causality assessment using the Naranjo probability scale revealed that the adverse drug event was probable. CONCLUSIONS: Bromocriptine was probably associated with DCMP in a patient being treated for a microprolactinoma. Severe DCMP needs to be considered a potentially life-threatening but reversible adverse effect of bromocriptine therapy for microprolactinoma of the pituitary gland.

Acute Disease↗
PubMed1985

[The effects of bromocriptine on anovulatory patients with high LH and euprolactinemia].

It is well known that an acute administration of Bromocriptine (dopamine agonist) suppresses the serum LH level either in normal women or in women with polycystic ovary syndrome, in whom the serum LH level is elevated. The present study was carried out to examine the effectiveness of Bromocriptine on anovulatory women with a high LH level (serum LH greater than 30 mIU/ml). Bromocriptine was administered for 3 months, 5 mg daily, to 9 anovulatory women with euprolactinemia (serum PRL less than 25 ng/ml). Ovulation was observed by their BBT charts. Before and after the treatment of Bromocriptine, FSH, LH and PRL secreting capacities were tested by LHRH and TRH injection. Also, estrone, estradiol and testosterone levels were measured before and after the Bromocriptine administration. Resting levels of LH, FSH and PRL were 45.4 +/- 11.0 mIU/ml, 11.4 +/- 3.0 mIU/ml, and 14.3 +/- 4.7 ng/ml (M +/- SD), respectively, before the treatment. As a result of the treatment, the LH level was markedly decreased to 27.3 +/- 14.5 (M +/- SD, P less than 0.05), and PRL decreased to 3.76 +/- 4.2 ng/ml (M +/- SD, P less than 0.005). On the other hand, FSH did not show a marked change. The responsiveness of LH to LHRH before the treatment showed a marked increase, which was suppressed by Bromocriptine. However, FSH showed no change. The responsiveness of PRL to TRH was suppressed by Bromocriptine. Serum estrone, estradiol and testosterone levels before the treatment were 115.5 +/- 76.7 pg/ml, 93.7 +/- 61.0 pg/ml and 0.809 +/- 0.209 ng/ml (M +/- SD), respectively, which showed no significant change after the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Effects of bromocriptine on endocrine environment in the polycystic ovary syndrome].

In order to investigate the hormone feature and the effect of bromocriptine on endocrine profile in patients with polycystic ovary syndrome (PCO), twenty-four-hour secretion pattern of LH, FSH, PRL and testosterone were assessed in 8 PCO patients and 4 normal women as controls by obtaining serial blood samples, taken through a forearm cannula, at 30 minute intervals for 24 hours. Bromocriptine, 5 mg/day was given and 3 patients were reassessed in the follicular phase of the menstrual cycle after ovulatory periods were established during bromocriptine therapy. There was significant difference in pulse amplitude, but not in pulse frequency of LH and testosterone between PCO and normal women (23.1 +/- 9.49 vs 5.75 +/- 1.28 mIU/ml, p less than 0.01; 27.8 +/- 10.1 vs 10.2 +/- 2.63 ng/dl, p less than 0.01), and the 24 hour mean LH and testosterone levels were higher (p less than 0.01) in PCO (52.3 +/- 20.1 mIU/ml, 105.1 +/- 15.9 ng/dl) than in normal women (13.4 +/- 4.31 mIU/ml, 54.3 +/- 13.3 ng/dl). Though a pulsatility in FSH secretion was identified, no difference between normal women and PCO was observed. Mean PRL level was within the normal range in PCO but with a higher pulse frequency (p less than 0.01) and lower pulse amplitude (p less than 0.01) than those of the normal women. Furthermore, LH and testosterone secretions maintained the circadian changes in PCO patients against the normal women. During bromocriptine therapy, mean level and pulse amplitude of LH and testosterone were significantly suppressed, without changing in pulse frequency, whilst PRL secretory patterns were not reestablished. In conclusion we have found that PCO is associated with high level and pulse amplitude of LH and testosterone, with high frequency and low amplitude of PRL, and bromocriptine administration can blunt LH, PRL and testosterone secretion, suggesting a hypothalamic intervention in gonadotropic regulation in patient with PCO. In addition, the degree of bromocriptine to inhibit LH secretion might be related to the dose or duration of its administration, or to the sensitivity of the patients. The mechanism of bromocriptine for marked LH suppression in PCO patients remains to be elucidated.

Adult↗
PubMed1985

Effect of bromocriptine on serum TSH in euthyroid patients with endocrine disorders.

In 10 euthyroid subjects a single 2.5 mg per os dose of bromocriptine caused rapid and remarkable decreases in serum TSH. As much as a 0.85 +/- 0.18 (s.d.) microU/ml decrease from the basal level (56 +/- 9%) was observed at 5 hours. A good correlation was observed between the basal TSH level and the TSH decrease after bromocriptine (r = 0.786). In 4 patients taking 5 to 15 mg bromocriptine daily (chronic administration group), another 2.5 mg bromocriptine also caused significant decreases in serum TSH, but the degree (0.42 +/- 0.03 microU/ml, 43 +/- 26% of basal) and duration (maximal at 4 hours) were less than those observed in the untreated group. The lowest TSH levels in these two groups did not differ significantly (0.80 +/- 0.45 and 0.78 +/- 0.53 microU/ml, respectively). The TSH decrease after bromocriptine in the untreated group was found not to correlate significantly with TRH induced TSH increase (r = 0.300). TRH induced TSH increase in the chronic administration group was similar to or greater than that of control subjects with matched basal TSH. The TSH lowering effects of per os prednisolone and triiodothyronine were also studied. Prednisolone exerted a quite similar effect to bromocriptine, but a certain time lag was observed in the case of triiodothyronine. A single dose of bromocriptine was found to lower serum TSH levels even in euthyroid subjects. The effect was considered to be independent of TRH-TSH regulation and to act directly on the TSH release.

Adult↗
PubMed1978

ACTH and cortisol response to bromocriptine, and results of long-term therapy, in Cushing's disease.

Plasma corticotrophin (ACTH) was lowered in 4 out of 5 patients with pituitary dependent Cushing's syndrome (one of whom was studied only after bilateral adrenalectomy) after a single oral dose of 2.5 mg bromocriptine, but plasma cortisols were unaltered in the 3 patients in whom it was measured. Three patients were observed during treatment with bromocriptine for 16 to 87 weeks. One improved symptomatically while maintained on a combination of metyrapone and bromocriptine, but plasma ACTH levels remained high even when the dose of bromocriptine was increased to 20 mg daily. Bromocriptine therapy was discontinued after 16 weeks in the second patient due to the development of mental depression. Her clinical features had not improved during this time. The third patient, who also underwent a course of pituitary irradiation, became, and remains, symptom free, with satisfactory plasma ACTH and cortisol levels for the 87 weeks he has received bromocriptine. The role of bromocriptine in the management of Cushing's disease seems limited despite the fact that plasma ACTH may fall after a test dose of the drug.

Administration, Oral↗
PubMed1985

Effects of bromocriptine on cell cycle distribution and cell morphology in cultured rat pituitary adenoma cells.

The effects of bromocriptine, a dopamine (DA) agonist, on cell cycle distribution and cell morphology have been studied in a clonal strain of rat pituitary adenoma cells (GH3) which produce and secrete spontaneously both prolactin (Prl) and growth hormone (GH). DNA flow cytometry showed that bromocriptine caused a dose-dependent delay in cell cycle traverse concomitantly with a reduction in cellular growth rate. The lowest concentration of bromocriptine (5 X 10(-6) mol/l) significantly (P less than 0.05) increased the relative number of cells in the S phase and reduced the proportion of cells in the G1 phase. At higher concentrations (1 X 10(-5)-5 X 10(-5) mol/l) bromocriptine delayed cell cycle traverse through effects on cells in the S, G1 and G2 phases. These effects occurred already after 24 h of treatment. These results were supported by autoradiography of nuclear uptake of [3H]thymidine and by measurements of the number of cells arrested in metaphase after colcemide treatment (mitotic rate). Bromocriptine at 5 X 10(-5) mol/l altered profoundly GH3 cell structure inducing cell clustering and typical changes in mitochondrial and nuclear ultrastructures. Since Prl and GH production is a characteristic of cells in G1 phase, the inhibitory effect of the lowest antiproliferative concentration of bromocriptine (5 X 10(-6) mol/l) can only partly be explained by alterations in phase distribution. At the highest concentration of bromocriptine (5 X 10(-5) mol/l) hormone production and cell division are also inhibited due to general toxic effects as reflected by the ultrastructural changes.

Adenoma↗
PubMed1986

Effects of bromocriptine on prolactin release, electrical membrane properties and transmembrane Ca2+ fluxes in cultured rat pituitary adenoma cells.

The effects of the dopamine (DA) agonist bromocriptine on prolactin (Prl) release, electrical membrane properties and transmembrane Ca2+ fluxes have been studied in a clonal strain of rat pituitary adenoma cells (GH3). These cells generate Ca2+ dependent action potentials, and produce and secrete spontaneously both Prl and growth hormone. Prl release stimulated by thyroliberin (TRH) and elevated extracellular K+ concentration was completely blocked by bromocriptine, whereas the basal release was only moderately affected. The TRH and K+ evoked Prl release were half maximally inhibited by bromocriptine at 5-10 and 10-50 microM, respectively. The normal biphasic membrane response to TRH and the depolarizing effect of elevated K+ concentration were not altered by bromocriptine, whereas the Ca2+- spikes in Na+-free solution were suppressed by the drug. We therefore suggest that bromocriptine blocks the voltage sensitive Ca2+-channels of GH3 cell. In agreement with this notion, bromocriptine also suppressed the basal and TRH induced 45Ca2+ efflux from preloaded cells. We conclude that the inhibitory effect of bromocriptine on the voltage dependent Ca2+- channels is an important mechanism responsible for suppression of Prl release.

Action Potentials↗
PubMed1991

Acute and long-term effects of once-daily oral bromocriptine and a new long-acting non-ergot dopamine agonist, quinagolide, in the treatment of hyperprolactinemia: a double-blind study.

Quinagolide (CV 205-502, Sandoz), an octahydrobenzo (g) quinoline, is a new non-ergot dopamine agonist which has specific D2 receptor activity and a long half-life, making it suitable for once-daily treatment. Recent uncontrolled reports have suggested that quinagolide may be successfully used for the clinical management of hyperprolactinemia with fewer adverse reactions than bromocriptine. This study is the first to compare quinagolide in a double-blind manner with bromocriptine, given only once-daily instead of the usual multidose regimen. In the first phase we compared, in 7 hyperprolactinemic patients, the effects over 24 h of a single oral dose of 0.05 mg quinagolide with 2.5 mg bromocriptine. Compared with placebo, both bromocriptine and quinagolide showed potent PRL-inhibiting and GH-releasing effects, with comparable effects at 24 h; no significant changes were observed in TSH, LH, FSH or cortisol. Twelve hyperprolactinemic patients were then randomized to receive either once-daily bromocriptine or quinagolide in incremental doses for a period of six months. Both drugs were found to be equally effective, and no differences were seen either in adverse reactions or PRL levels during repeated diurnal sampling. We therefore conclude that quinagolide and bromocriptine are therapeutically equivalent in long-term use, and both are equally effective when given once a day. However, some patients intolerant of bromocriptine may respond better to quinagolide, and vice versa.

Adult↗
PubMed1992

Bromocriptine treatment over 12 years in acromegaly: effect on growth hormone and prolactin secretion.

It is not known whether bromocriptine treatment in acromegaly can be implemented for a life-long period. To elucidate this problem, the secretory GH and PRL states of 12 patients with acromegaly were determined, before bromocriptine treatment, under therapy (15.0 +/- 6.8 mg/day for 12 +/- 3 years; mean +/- SD) and during two-weeks long drug withdrawal after long-term treatment, respectively. Before therapy, all patients showed a non-sufficient GH suppression after oral glucose load (greater than 2 micrograms/l), whereas under dopaminergic treatment the post-glucose GH levels of three patients fell below 2 micrograms/l; normal IGF-I concentrations were found in five patients. However, under bromocriptine, only two patients showed GH suppressions below 2 micrograms/l following glucose, accompanied with normal IGF-I levels. During bromocriptine withdrawal, GH secretion at 60 min in the oral glucose tolerance test increased significantly (17.0 +/- 15.5 vs 5.7 +/- 5.2 micrograms/l; p less than 0.01); the mean IGF-I level rose from 2.1 +/- 0.8 to 4.9 +/- 2.2 kU/l (p less than 0.01). IGF-I was normal during bromocriptine cessation in only one patient; none of the 12 patients showed a GH suppression below 2 micrograms/l after oral glucose load. Under dopaminergic treatment hyperprolactinemia could not be detected. In conclusion, bromocriptine led to a stable suppression of both GH hypersecretion and--if present--concomitantly elevated PRL levels. Severe side effects or a further tumor growth could not be observed. Thus, the data of the longest follow-up investigation that has so far been published indicate that effective life-long bromocriptine therapy seems to be possible in selected patients with acromegaly.

Acromegaly↗