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PubMed1980

The use of bromocriptine for testing central dopaminergic reactivity.

A single oral intake of 10 mg of Bromocriptine can modify both plasma renin activity (PRA) and arterial blood pressure (BP). The changes in both variables depend on the integrity of the central dopaminergic systems. The parkinsonians whose extrapyramidal symptoms are markedly improved by L-Dopa in association with a decarboxylase inhibitor (IDC) and the untreated parkinsonians are the only patients whose PRA and BP are lowered 1 h after Bromocriptine ingestion. The results obtained in the L-dopa-induced dyskinetic parkinsonians are similar to those obtained in the group of L-Dopa-resistant patients. This points to the paradoxical hypothesis of dopaminergic hyposensitivity in the dyskinetic patients. In spite of the absence of correlation between PRA and BP, it is possible that lowering of BP by Bromocriptine is linked to the parallel decrease of PRA. An increase of the BP may be obtained in the dyskinetic and L-Dopa-resistant groups. These data point to a possible involvement of central dopaminergic systems in some aspects of hypertension.

Blood Pressure↗
PubMed1983

Effect of low-dose bromocriptine in treatment of psychosis: the dopamine autoreceptor-stimulation strategy.

Bromocriptine (0.5-6.0 mg/day) was administered to seven unmedicated chronic schizophrenic and two schizoaffective patients. Transient slight improvement was noted in four patients and marked improvement in one other. Clinical improvement was associated with nausea and drowsiness. These doses of bromocriptine stimulated serum growth hormone and inhibited serum prolactin levels in some subjects. These results suggest that bromocriptine may stimulate dopamine autoreceptors and, through this mechanism, attenuate symptoms in a small proportion of psychiatric patients.

Brain Chemistry↗
PubMed1982

The effect of chronic bromocriptine and L-dopa on spiperone binding and apomorphine-induced stereotypy.

Chronic treatment with dopamine (DA) agonists has been reported in various paradigms to cause supersensitivity of DA receptors or, contradictorily, subsensitivity of DA receptors. The present study administered 15 mg/kg bromocriptine for 7 days and measured both striatal spiperone binding and apomorphine (AP)-induced stereotypy. A significant decrease in AP-induced stereotypies was observed after chronic bromocriptine treatment, but without a significant parallel decrease in striatal spiperone binding. These results probably do not represent a true agonist-induced subsensitivity, but possibly show that residual bromocriptine in vivo may antagonize AP-induced stereotypy. Since some reports have suggested that L-Dopa may specifically reverse the increases in DA receptor number induced by chronic haloperidol, we also studied the effect of 7 days of L-Dopa treatment after 6-week chronic haloperidol treatment of mice. While chronic haloperidol significantly increased striatal spiperone binding, subsequent L-Dopa treatment did not reverse this biochemical supersensitivity. It is concluded that agonist induction of subsensitivity in the DA system is difficult to reproduce and may depend on highly specific dosage conditions and treatment schedules.

Animals↗
PubMed1979

Hypothermic action of lisuride in rats and differences to bromocriptine in the antagonistic effect of neuroleptics.

The semisynthetic ergot derivative lisuride induced dose- and time-dependent hypothermia in rats placed in a cold environment (+4 degrees C). As regards dosage, lisuride was more than 100 times more effective in this test model than bromocriptine. The effect of both drugs could be reduced by pretreatment with the dopamine antagonist haloperidol, which indicated a dopaminergic action of both drugs. In contrast, the hypothermic effect of lisuride could not be impaired by pretreatment with sulpiride, whilst the effects of bromocriptine were clearly antagonized by this drug. This results could be explained by a different affinity of these drugs to the same receptors, or, more likely, by a different mechanism of action by which lisuride and bromocriptine activate dopaminergic systems.

Animals↗
PubMed1982

Metergoline versus bromocriptine in the prevention of puerperal lactation. A double-blind clinical trial.

In a double blind study of the prevention of puerperal lactation, the clinical efficacy of two antiprolactin drugs was compared: metergoline 4 mg tid and bromocriptine 2.5 mg bid were both given for 7 days. An additional 7 days of treatment was administered to 16 patients in whom mammary activity was still present or appeared in the following 3 days. The first 7 day period of treatment was effective in 16/20 women receiving metergoline and in 7/20 on bromocriptine (p less than 0.02); the second period of treatment was effective in all remaining patients. These data indicate that metergoline acts rapidly to arrest puerperal lactation, possibly by a mechanism different from that of bromocriptine.

Bromocriptine↗
PubMed1985

Bromocriptine reduces plasma noradrenaline and 3,4-dihydroxyphenylacetic acid in normal and hypotensive subjects.

The effect of a single oral dose of bromocriptine 2.5 mg was evaluated in 11 normotensive and 6 hypertensive volunteers. 150 min after drug administration, a significant decrease in plasma noradrenaline concentration from 202 to 124 pg/ml in normotensive and from 197 to 119 pg/ml in hypertensive patients was observed. Plasma 3,4-dihydroxyphenylacetic acid, a major metabolite of dopamine, fell from 1132 to 956 pg/ml in normal subjects and from 1242 to 807 pg/ml in hypertensives. No change in plasma adrenaline was found. At the same time, mean arterial pressure showed a significant decrease from 90 to 81 and from 132 to 111 mmHg in normotensive and hypertensive subjects, respectively. Bromocriptine also inhibited the increase in noradrenaline level that occurred when the subjects changed from the supine to the standing position. The inhibition was more evident in hypertensive subjects. It is suggested that the hypotensive effect of bromocriptine is mediated by the inhibition of noradrenaline release due to the stimulation of dopamine receptors on noradrenergic nerve terminals.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Differential effect of food on kinetics of bromocriptine in a modified release capsule and a conventional formulation.

The influence of food on release of drug from a modified release capsule of bromocriptine 5 mg (Parlodel SRO) and a conventional formulation of bromocriptine 5 mg has been studied in 8 healthy male volunteers. Both formulations produced objective and subjective effects, such as orthostatic reactions, nausea, dizziness, vomiting and nasal congestion. The modified release capsule caused fewer side-effects than the normal capsule. Both formulations had less cardiovascular effect in the fed than in the fasting state. There was no significant difference between the normal and the modified release capsules taken fasting or after a meal in terms of the AUC extrapolated to infinity. The relative bioavailability of the 5 mg modified release capsule was 84.6% of the normal capsule under fasting conditions and 107.5% after food. In contrast to the virtually unchanged extent of absorption, the rate of absorption was markedly affected by food, especially from the conventional capsule. The mean time of 50% absorption increased from 1.06 h (fasting) to 3.2 h (fed), whereas for the modified release capsule food mainly resulted in an increased lag time of absorption. The almost instantaneous dissolution of bromocriptine from the normal capsule in vitro (both in HCl and fasting human gastric juice) and the delay of absorption after a meal in vivo suggest that the rate limiting step in absorption of the normal capsules is delivery of released drug from the stomach to the small intestine, which is delayed by food. Both the modified release 5-mg capsule and the normal 5-mg capsule showed extended suppression of prolactin over 36 h, in all subjects, both fasted and after a meal.

Adult↗
PubMed1985

Mesulergine and bromocriptine in long-term treatment of advanced parkinsonism.

24 levodopa pretreated patients with advanced parkinsonism were split into two equal groups receiving mesulergine or bromocriptine respectively as an adjuvant therapy. The trial was carried out under double blind conditions the first three months and then continued as an open trial for one year. Clinical benefit was similar in both groups with minor differences in regard to single symptoms. While bromocriptine showed a beginning decline in efficacy after one year, mesulergine showed no decline. The mean mesulergine-dose, necessary to achieve good clinical improvement, was about half of bromocriptine. Side-effects were similar, except orthostatic hypotension requiring vasopressor medication, which was less frequent in mesulergine treated patients. This advantage of mesulergine might be explained by its special pharmacological pattern with biphasic action on dopaminergic receptors.

Adult↗
PubMed1981

Recent advances in the treatment of Parkinson's disease: the role of bromocriptine.

We have treated 102 Parkinson patients with bromocriptine for up to 6 years; most of these posed problems of management when referred to us. Forty-two continue to take bromocriptine, at a mean dose of 49 mg daily (range 10-160), in combination with some 50% of their previous optimal dose of levodopa (with or without a decarboxylase inhibitor). We consider the main indications for bromocriptine are severe dyskinesia, early morning dystonia, and "wearing off" reactions. Contraindications include hallucinations, delusions, substantial confusion, acute myocardial infarction, active peptic ulceration, and active pleuropulmonary disease.

Bromocriptine↗
PubMed1978

Plasma pituitary hormones in patients with Parkinson's disease treated with bromocriptine.

Bromocriptine was used for Parkinson's disease in 15 patients for 20 weeks. Immunoreactive plasma lutrophin (LH), follitrophin (FSH), prolactin, and somatotrophin (GH, growth hormone) concentrations were analysed before and during the treatment. Plasma prolactin levels were very markedly reduced during treatment. Plasma lutrophin levels were increased significantly in female patients, but not in male patients. No changes were noticed in follitrophin levels, but plasma somatotrophin levels were reduced during treatment. No correlations were found between the degree of clinical response and changes in plasma gonadotrophin and somatotrophin. This suggests that the effects of bromocriptine on extrapyramidal and neuroendocrine dopaminergic neurones are unrelated. We suggest careful and frequent controls of neuroendocrine secretion patterns in patients with Parkinson's disease who are treated with high doses of dopamine receptor stimulators, since the response of some pituitary hormones to bromocriptine are very marked.

Aged↗
PubMed1995

Bromocriptine and suppression of postpartum lactation. The incidence of adverse cardiovascular effects in women of child-bearing age.

The use of bromocriptine for the suppression of postpartum lactation drew widespread attention to a potentially increased risk for cardiovascular and cerebrovascular adverse effects. To estimate the incidence of these events a follow-up study was performed among 2,130 women of 15-44 years of age who were treated with a course of bromocriptine in 1990-1992. None of these women were admitted to the hospital for cardiovascular or cerebrovascular events. However, the incidence of pregnancy hypertension and the use of cardiovascular drugs increased considerably in the last 2 months before delivery. Therefore, cardiovascular or cerebrovascular events can probably be explained by pre-existing morbidity rather than by the use of bromocriptine. We estimated, using a 'worst-case' analysis, that fewer than 2 Dutch women each year would develop serious cardiovascular or cerebrovascular events.

Adolescent↗
PubMed1982

The serum levels of testosterone and prolactin in patients with prostatic carcinoma treated with various doses of Fostrolin and bromocriptin.

In 45 patients with newly diagnosed carcinoma of the prostate, 1509 radioimmunological assays (RIA) were done for serum testosterone (T), prolactin (PRL) and growth hormone (GH). The patients were divided into 4 groups and treated with gradually lowered doses of Fostrolin and bromocriptin. It was noted that after high doses of Fostrolin, T levels did not markedly decrease, and PRL concentrations increased manifold. Small doses of Fostrolin, however, caused a drop in T and PRL levels. In the light of the results of up-to-date investigations and of the role played by PRL in a higher incidence of prostatic tumours, employment of bromocriptin, a prolactin antagonist, in the treatment of prostatic cancer seems to be justified. Reduction of T concentration below castration level and attainment of trace PRL levels in response to small doses of Fostrolin and bromocriptin had a favourable effect on the clinical course of the malignant disease.

Antineoplastic Agents↗
PubMed1987

Long term treatment with oral single administration of bromocriptine in patients with hyperprolactinemia.

In the treatment of hyperprolactinemia bromocriptine is generally administered in 3 daily doses during the day. Due to the limited compliance of patients under this long term regimen, in 16 hyperprolactinemic patients we investigated the efficacy and tolerability of the treatment with this dopaminergic drug administered as a single evening dose. This dose was the same which the patients had been assuming previously on a tid basis. Chronic treatment (4-12 months) with an oral single evening dose of bromocriptine is able to control plasma PRL at least as well as the traditional tid regimen (2.8-21.6 ng/ml vs 1.2-31.8 ng/ml). Furthermore, during this single dose regimen the side effects were of lesser intensity and extent. Since the compliance of the patients with the single dose regimen was very good and the efficacy the same in reducing plasma PRL and controlling the clinical manifestations with a lower rate of side effects, we suggest to extend this regimen to all patients with hyperprolactinemia treated with bromocriptine after successful reduction of plasma PRL levels is obtained.

Administration, Oral↗
PubMed1986

Effect of bromocriptine on plasma catecholamines in normal subjects and prolactin-secreting tumor patients.

The effect of short term bromocriptine (5 mg/day, 5 days) on plasma epinephrine (E), norepinephrine (NE), dopamine (DA) and prolactin (PRL) was studied in 4 normal women and 6 bearing PRL-secreting tumors. When studied on placebo no significant differences were found between controls and patients in E, NE and DA plasma levels. Bromocriptine induced: a 70% decrease in PRL levels in both groups, a significant (p less than 0.05) decrease in plasma NE levels in the control group, no significant change in plasma NE levels in the hyperprolactinemic patients when considered as a group. These results do not indicate that bromocriptine is a useful tool in the diagnosis of defective central dopaminergic regulation since individual responses of the PRL-secreting tumor patients were variable. Nevertheless, the impaired response of the group as a whole may be suggesting an underlying alteration of DA2 receptor activity in these tumor patients.

Adolescent↗
PubMed1987

Acute effects of L-dopa and bromocriptine on serum PRL, LH and FSH levels in patients with hyperprolactinemic and normoprolactinemic polycystic ovary syndrome.

We have investigated the importance of the dopaminergic control of gonadotropin secretion by studying LH, FSH and PRL responses to L-dopa and bromocriptine in patients with polycystic ovary syndrome (PCOS). Both L-dopa and bromocriptine administration were followed by a statistically significant decrease in LH in the hyperprolactinemic PCO patients (compared to the normoprolactinemic subgroup - p less than 0.01 and control group - p less than 0.05); the decline was proportional to the basal level of LH. A significant positive correlation between basal LH levels and maximum net decrease of LH was observed after administration of both agents (p less than 0.01). Although both subgroups of PCO patients showed a similar decrease in PRL levels it was statistically significant only in the normoprolactinemic patients (p less than 0.01). Prolactin sensitivity to the inhibitory effect of bromocriptine and L-dopa showed a significant correlation with the basal PRL level (p less than 0.01). The response of serum FSH was variable and not significant. These results suggest that a reduction of an inhibitory influence of hypothalamic dopamine might be a cause of inappropriately elevated LH and PRL levels found in patients with polycystic ovary syndrome and hyperprolactinemia.

Adult↗
PubMed1984

Bromocriptine-induced regression of a suprasellar extending prolactinoma during pregnancy.

A 21-year-old amenorrheic woman with hyperprolactinemia had rapid pituitary tumor enlargment during a bromocriptine-induced pregnancy. Before treatment the sella turcica was normal. In the 31st week of pregnancy she developed bitemporal hemianopsia and markedly decreased visual acuity. Computerized tomography showed a pituitary adenoma with suprasellar extension. Reinstitution of bromocriptine therapy resulted in rapid recovery of normal vision and radiologically verified tumor regression. Pregnancy continued to term and a healthy child was born. If pituitary tumor complications should occur during pregnancy, reinstitution of bromocriptine is the primary treatment of choice.

Adult↗
PubMed1990

Bromocriptine reduces rat thyrotropin beta-subunit mRNA stability.

We have examined the effect of orally administered bromocriptine on TSH beta-subunit messenger (m)RNA in the anterior pituitary glands of Sprague-Dawley rats using in situ and dot-blot hybridization histochemistry. Quantitative in situ hybridization of pituitary sections demonstrated a 60% reduction in TSH beta-subunit mRNA probe binding from rats fed a diet containing bromocriptine 10 mg/kg/day. This was confirmed by dot-blot analysis of nuclear and cytoplasmic pituitary extracts from the same tissue. Hybridization of cytoplasmic extracts of pituitary cells cultured under actinomycin D-induced transcription arrest showed that part of the effect of bromocriptine appeared to be mediated through a change in TSH beta-subunit mRNA stability and implies that the acute influence of dopamine on TSH metabolism may be transduced by control of TSH beta-subunit mRNA catabolism. This suggests a mechanism by which cells with relatively stable tissue specific mRNAs appear to respond rapidly to hormonal effects at the transcriptional level.

Administration, Oral↗
PubMedDate not supplied

The mechanism of the effect of combination treatment with clomiphene and bromocriptine in patients with normoprolactinemic anovulation.

The combination treatment with bromocriptine and clomiphene citrate was applied to 11 normoprolactinemic anovulatory patients who did not respond to clomiphene citrate alone. This combination treatment restored ovulation in 8 of these patients (72.7%). Conception was observed in 2 patients (18.1%) out of 11. The patients who responded to combination treatment showed a significant increase in the serum level of estradiol in the preovulatory phase, of progesterone in the mid-luteal phase, and a significant decrease of serum prolactin. They also showed significant increase in the frequency of luteinizing hormone (LH) pulsatility on day 12 of the cycle from 1.38 +/- 0.86 to 3.75 +/- 0.83 pulses/4h. The 3 patients who did not respond to combination treatment showed no increase in the serum level of estradiol or progesterone, but showed increase in the frequency of LH pulsatility in spite of continuous anovulation. These results indicate that the combination treatment with bromocriptine and clomiphene citrate is effective for treatment of patients with normoprolactinemic anovulation who do not respond to clomiphene alone, and suggest that the mechanism of the effect of combination treatment is related to an increase in the frequency of LH pulsatility caused by bromocriptine, which in turn stimulates follicular maturation.

Adolescent↗