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PubMed1997

Continuous bromocriptine therapy in menstrual migraine.

This investigation assessed the effects of an open, prospective trial of adjunctive continuous bromocriptine therapy on the frequency of refractory, disabling menstrual migraine. It compared continuous bromocriptine with previously optimal baseline therapy and cyclic perimenstrual bromocriptine use. The subjects were 24 women with disabling migraines that occurred exclusively or at least 50% of the time within 3 days before or after the onset of menstruation despite treatment. We added bromocriptine 2.5 mg three times a day to their existing regimen and compared menstrual migraine frequency during the first year with the year prior to bromocriptine. Eighteen of the 24 women experienced a 25% or greater decline in migraine frequency. Migraine frequency declined by 72% overall (p < 0.01). Three women did not tolerate bromocriptine, and three did not benefit. None of the women had a 10% or greater increase in headaches. Continuous bromocriptine therapy was also significantly more effective than intermittent bromocriptine use (p < 0.05). Continuous bromocriptine therapy appears to benefit menstrual migraine.

Adult↗
PubMed1993

[A study with diagnostic standard of occult hyperprolactinemia (OHP) and the effect of bromocriptine administration].

It is well known that the transient excessive increase of serum prolactin level is harmful for the mechanism of ovulation or the steroidogenesis of the ovaries. The pathogenesis of latent or occult hyperprolactinemia (OHP) has been investigated recently. The present study was conducted to determine the diagnostic standard of OHP, and to elucidate the efficacy of bromocriptine administration for the treatment of OHP and other ovulatory disturbances. 110 cases of hypothalamic anovulations were selected from 385 cases of infertile patients by the LH-RH and TRH loading tests. Bromocriptine (5mg/day) was administered to all of the subjects for more than three months, and the efficacy of the bromocriptine administration was investigated. Follicular development was observed by transvaginal ultrasonography (mature follicular diameters > or = 20mm), and also luteal function was estimated by the duration of the luteal phase in the BBT charts (high phase > or = 12 days), the mid-luteal serum estradiol (> or = 200pg/ml) and progesterone (> or = 10ng/ml) levels. The subjects were divided into two groups: group A, bromocriptine effective patients (63 cases) and group B, bromocriptine non effective patients (47 cases). The results of the LH-RH and TRH loading tests were compared between these two groups. Serum prolactin levels at 30 min. after TRH loading (PRL30) in group B (61.5 +/- 28.3 vs. 38.0 +/- 19.3ng/ml, p < 0.01). At the cut-off points of 50, 60 and 70ng/ml over in the values of the PRL, the efficacies of the bromocriptine administration were 77.4, 78.9 and 88.5%, respectively. From these facts, it was thought suitable that the diagnostic standard of OHP was PRL30 > or = 70ng/ml, and values of PRL30 from 50 to 70ng/ml were borderline cases of OHP. The efficacy of the bromocriptine administration in the cases without OHP (n = 57) was also investigated. Serum LH levels at 30 min. after LH-RH loading (LH30) were compared between the cases of the bromocriptine effective (n = 22) and non effective (n = 35). As a result, the LH30 of the former was significantly higher than that of the latter (96.5 +/- 64.2 vs. 45.1 +/- 31.5mIU/ml, p < 0.005). In conclusion, the diagnostic standard of OHP was determined as PRL30 > or = 70ng/ml (borderline: 50 > 70ng/ml), and bromocriptine administration was effective not only in cases of OHP, but also in cases of hyperreactivities of LH (so-called endocrinological PCOD).

Anovulation↗
PubMed1999

Bromocriptine-induced premature oestrus is associated with changes in the pulsatile secretion pattern of follicle-stimulating hormone in beagle bitches.

The secretory profiles of LH and FSH were investigated before and during the administration of bromocriptine in six beagle bitches. Plasma samples were obtained via jugular venepuncture at 10 min intervals for 6 h every 2 weeks until the next ovulation. Bromocriptine treatment was started 100 days after ovulation. Both before and after bromocriptine treatment, LH and FSH pulses occurred together. The mean duration of the FSH pulse (120 min) was significantly longer than that of the LH pulse (80 min). The interoestrous interval in the bitches treated with bromocriptine was significantly shorter than that of the preceding cycle (160 +/- 3 versus 206 +/- 24 days). The mean basal plasma FSH concentration (7.4 +/- 0.6 versus 6.1 +/- 0.7 iu l-1) and the mean area under the curve for FSH (46.6 +/- 4.7 versus 40.4 +/- 4.4 iu l-1 in 6 h) increased significantly after the start of the bromocriptine treatment. In contrast, the differences in mean basal plasma LH concentration (2.1 +/- 0.2 versus 2.0 +/- 0.2 micrograms l-1) and the mean area under the curve for LH (19.0 +/- 3.1 versus 19.5 +/- 2.5 micrograms l-1 in 6 h) between the day before and 14 days after the start of the bromocriptine treatment were not significant. Bromocriptine administration also lowered the mean amplitude of the FSH pulse and shortened the mean duration of the FSH pulse, without influencing the LH pulse. In addition to demonstrating the concurrent pulsatile secretion of LH and FSH, the results of the present study demonstrate that the bromocriptine-induced shortening of the interoestrous interval in the bitch is associated with an increase in plasma FSH concentration without a concomitant increase in plasma LH concentration. This finding indicates that treatment with the dopamine agonist bromocriptine increase plasma FSH to a concentration that results in the enhancement of follicle development.

Analysis of Variance↗
PubMed1994

Effects of bromocriptine treatment on the expression of sexual behavior in male sheep (Ovis aries).

Twenty-three rams were treated twice daily with subcutaneous injections of bromocriptine or vehicle over 30 d during two seasons, spring and fall. Sexual behavior was observed and quantified to determine the effects of bromocriptine-induced hypoprolactinemia on mount attempt (MA), mount (M), and ejaculation (E) frequency of the rams upon exposure to estrous ewes. Behavioral responses and serum prolactin (PRL) concentrations were determined on a weekly basis before, during, and after the treatment period in each season. Treatment with bromocriptine caused a significant decrease in serum concentrations of PRL during both seasons (P < .01). Post-treatment period concentrations of PRL returned to pretreatment levels during the spring, whereas during the fall, post-treatment period PRL concentrations remained low (P < .05). The frequency of MA and M was lower during bromocriptine treatment relative to control rams in the spring (P < .05). The frequency of MA and M returned to pretreatment values after bromocriptine treatment was withdrawn. Ejaculation frequency tended to decrease during and after bromocriptine treatment relative to controls (P < .09). There was no effect of bromocriptine treatment on frequency of MA and M during the fall. During the fall, the frequency of E tended to decrease in bromocriptine-treated rams (P < .1). These data indicate that bromocriptine-induced hypoprolactinemia is associated with a significant diminution in expression of sexual behavior in rams. It is suggested that PRL modulates the intensity of expression of sexual behavior in rams, and this effect may be season-dependent.

Animals↗
PubMed1984

Clinical and pathological effects of bromocriptine on prolactin-secreting and other pituitary tumors.

Bromocriptine inhibits prolactin secretion and causes size reduction of prolactin-secreting adenomas. The effect of the drug upon pituitary tumors other than prolactinomas is uncertain. The authors report a prospective series of 12 patients with pituitary macroadenomas in whom bromocriptine was administered for 6 weeks prior to transsphenoidal surgery. Five of the patients had computerized tomographic documentation of significant reductions in tumor size (Group A) and six had no change (Group B) during 3 and 6 weeks of bromocriptine administration. One patient who demonstrated size reduction in his tumor was not assigned to either group as he was treated with high-dose dexamethasone concurrently with the bromocriptine. Pathological examination (light and electron microscopy and immunocytochemistry) indicated that all Group A patients harbored tumors with prolactin granules whereas all Group B tumors lacked such granules. Adenoma cells in the responsive tumors were involuted with reduced cytoplasmic, nuclear, and nucleolar areas. Neither widespread cell necrosis, infarction, nor vascular injury was observed. Two of the five Group A patients discontinued bromocriptine prior to completion of the 6-week protocol and had a rapid return of their tumors to pre-treatment size. Although bromocriptine has been reported to cause shrinkage of nonfunctional tumors, there was no radiological evidence of size reduction or pathological changes in the nonfunctional tumors of this series. Interestingly, serum levels of prolactin were modestly elevated (84 and 113 ng/ml) in two of the six Group B patients, an elevation due to stalk compression rather than secretion by adenoma cells. This finding underscores the fact that failure of bromocriptine to reduce pituitary tumor size in the presence of hyperprolactinemia may occur because the tumor is other than a prolactinoma. This is the first moderate-sized group of patients in whom pathological changes in responsive prolactinomas during bromocriptine therapy have been demonstrated. As bromocriptine is not tumoricidal, and thus not curative, there is insufficient evidence to recommend this drug as primary therapy for either prolactin-secreting or nonfunctional macroadenomas, but the drug may have potential as a preoperative adjunct to effect shrinkage of prolactinomas and theoretically, at least, make excision easier and possibly more complete.

Adenoma↗
PubMedDate not supplied

A clinical study of taxotere versus taxotere plus the antiprolactinemic agent bromocriptine in metastatic breast cancer pretreated with anthracyclines.

Prolactin (PRL) constitutes a growth factor for breast cancer cell proliferation and abnormally elevated blood concentrations of PRL are associated with poor prognosis and reduced efficacy of antitumor therapies in metastatic breast carcinoma. It has already been demonstrated that low-dose bromocriptine, an antiprolactinemic long-acting dopaminergic drug, normalizes PRL blood concentrations in metastatic breast cancer patients with abnormally elevated PRL levels. In addition, previous clinical studies have already demonstrated a lower efficacy of chemotherapy with taxotere in metastatic breast cancer, with persistent hyperprolactinemia. We planned a controlled clinical study to evaluate the influence of a concomitant administration of the antiprolactinemic drug bromocriptine on the efficacy of chemotherapy with taxotere, in metastatic breast cancer patients progressing after chemotherapeutic combinations containing anthracyclines. The study included 30 randomized consecutive patients treated with taxotere alone or taxotere plus bromocriptine. Taxotere was given I.V. at 100 mg/m2 every 21 days for 3 cycles. Bromocriptine was given orally at 2.5 mg/day every day until the end of the chemotherapeutic treatment. Bromocriptine therapy induced a significant decline in PRL mean blood concentrations compared to patients treated by chemotherapy alone. No complete response was obtained. A partial response (PR) occurred in 5 out of 14 (36%) patients treated with taxotere plus bromocriptine and in only 2 out of 16 (13%) patients treated with taxotere alone. Moreover, a stable disease (SD) was obtained in 5 out of 16 patients treated with taxotere alone and in 7 out of 14 patients concomitantly treated with bromocriptine. Therefore, the percent of non-progressive disease (PR + SD) achieved in patients treated with taxotere plus bromocriptine was significantly higher with respect to that found in patients treated with taxotere alone (12 out of 14 vs 7 out of 16, p < 0.025). This preliminary clinical study would suggest that the inhibition of PRL secretion by antiprolactinemic drugs such as bromocriptine may enhance the efficacy of chemotherapy for metastatic breast cancer.

Aged↗
PubMedDate not supplied

Bromocriptine decreases blood pressure of spontaneously hypertensive rats without affecting the adrenomedullary synthesis of catecholamines.

Because of controversial data on the role of adrenomedullary catecholamines (CA) in the hypertension of spontaneously hypertensive rats (SHR) and in the hypotensive action of bromocriptine, we studied the effect of chronic bromocriptine treatment on blood pressure (BP), adrenal CA synthesis, tissue CA, and urinary excretions of CA and their metabolites in SHR. We found that the hypertension of 12-week-old SHR (systolic BP, 181 +/- 13 mm Hg) was reduced to 123 +/- 8 mm Hg when they received bromocriptine between 4 and 12 weeks of age (2 X 600 micrograms/kg/day, intraperitoneally). Although the urinary epinephrine (E) and the synthesis of adrenal norepinephrine (NE), E, and dopamine (DA), as well as the tissue content of CA in adrenals, heart, and kidney, remained unchanged after bromocriptine treatment, the urinary NE and DA excretions were lower in bromocriptine-treated SHR than in sham-treated SHR (NE, 2.7 +/- 0.3 versus 4.2 +/- 0.3 nmol/24 h in control SHR; DA, 18.7 +/- 1.6 versus 28.2 +/- 2.2 nmol/24 h in control SHR). In SHR, bromocriptine treatment did not affect the previously observed selectively increased adrenal turnover and synthesis of DA or the urinary excretions of normetanephrine (NM), dihydroxyphenylacetic acid (DOPAC), 3-methoxytyramine (3-MT), or homovanillic acid (HVA). The results suggest that the bromocriptine-induced decrease of BP in SHR is not mediated by changes in adrenomedullary CA and that bromocriptine decreases the BP of SHR without affecting the previously observed increased adrenal DA release of SHR. Thus, other central or peripheral dopaminergic agonist actions of bromocriptine bypassing the adrenal medulla must be considered in the hypotensive action of the drug.

Adrenal Medulla↗
PubMed1987

[Indication and effect of bromocriptine in euprolactinemic amenorrhea--comparison with clomiphene].

Effect of bromocriptine on induction of ovulation and occurrence of pregnancy was examined in patients with normoprolactinemic ovulatory disturbances. The patients under study (53 in number) were divided into two groups, A and B, depending on the effect clomiphene had on the ovulatory responses and the occurrence of pregnancy. Of the group A, patients (21 in number), who had failed to show any ovulatory response to clomiphene, 8 patients ovulated on bromocriptine alone. Three out of 13 patients who complained of sterility became pregnant. Three out of 8 patients who had not ovulated on bromocriptine therapy alone ovulated on a combination of bromocriptine and clomiphene, and 2 out of these 3 cases became pregnant. Of the group B patients (31 in number), who had failed to become pregnant in spite of ovulatory responses to previous clomiphene therapies, 7 out of 23 became pregnant, who complained of sterility when on bromocriptine alone. Out of 12 cases who had failed to get pregnant on the bromocriptine alone, 2 patients became pregnant on the combination of bromocriptine and clomiphene. These data may indicate that the bromocriptine or the combined therapy of bromocriptine and clomiphene is useful for the treatment of patients with ovulatory disturbances or sterility who do not respond to the clomiphene therapy.

Adult↗
PubMed1986

Cytosuppressive effect of bromocriptine on human prolactinomas: stereological analysis of ultrastructural alterations with special reference to secretory granules.

To ascertain the mechanisms of bromocriptine in lowering serum prolactin (PRL) levels and reducing the cell size of human prolactinomas, stereological analysis at electron microscope level was performed on six adenomas treated with bromocriptine (10 mg/day for 2 weeks) and four untreated adenomas. The bromocriptine treatment significantly decreased all the major organelles involved in PRL synthesis when expressed in absolute volume per single tumor cell, although it decreased only Golgi apparatus when expressed in relative volume within the cells. Secretory granules, lysosomes, and lipid droplets increased in relative volume but not in absolute volume in bromocriptine-treated adenomas. Consequently, bromocriptine decreased the volume of individual tumor cell to approximately 60% of that of untreated tumor cells. Unexpectedly, exocytosis of secretory granules increased significantly in the bromocriptine-treated adenomas in spite of a remarkable decrease in serum PRL levels. This appears to be contradictory to the current view that a decrease in serum PRL levels with a concurrent increase in the intracellular PRL levels caused by bromocriptine treatment results from the inhibition of exocytosis of secretory granules. The secretory granules of bromocriptine-treated adenomas may contain a small amount of PRL, as suggested by a culture study reporting degradation of PRL by bromocriptine.

Adenoma↗
PubMed1976

Bromocriptine treatment in Parkinson's disease.

Thirty-one patients with Parkinson's disease were treated with the ergot alkaloid bromocriptine, a drug which stimulates dopamine receptors. Bromocriptine had a slight therapeutic effect in patients on no other treatment and an additional effect in patients on levodopa. The mean optimum dosage of bromocriptine, established over a 12 week period, was 26 mg daily. In 20 patients bromocriptine was compared with placebo in a double-blind controlled trial. Active treatment caused a significant (P less than 0.02) reduction in total disability and akinesia scores. The least disabled patients showed the greatest response. Side-effects of bromocriptine--nausea, vomiting, hallucinations, and abnormal involuntary movements--were similar to nature to those of levodopa. In most normal subjects, bromocriptine causes an increase in plasma growth hormone concentration. This was determined in 20 patients with Parkinson's disease after 1-15 mg bromocriptine. Only a single patient showed an obvious increase up to 120 minutes after dosage. Bromocriptine was not effective treatment in two patients who had not previously responded to levodopa and replacement of this drug by bromocriptine in patients with end-of-dose akinesia after chronic levodopa treatment did not totally abolish response swings.

Aged↗
PubMed1994

Pergolide compared with bromocriptine in Parkinson's disease: a multicenter, crossover, controlled study.

We compared the efficacy and safety of pergolide and bromocriptine in 57 patients with Parkinson's disease (PD) with a declining response to levodopa therapy in a single-blind, crossover study. Patients were placed randomly on the sequence bromocriptine-pergolide (12 + 12 weeks) or vice versa. Regular evaluations using the New York University Parkinson's Disease Scale were performed by a clinician blinded to treatment assignment. Patients' and clinicians' impressions also were recorded. The average daily dose of pergolide was 2.3 +/0- 0.8 mg, and that of bromocriptine was 24.2 +/- 8.4 mg. Significantly greater efficacy was demonstrated by both drugs as adjunctive therapy to levodopa compared with previous treatment of levodopa alone (pergolide, p = 0.0001; bromocriptine, p = 0.0005; Wilcoxon t test). Pergolide was more effective than bromocriptine in daily living scores (p = 0.020) and motor scores (p = 0.038). No difference in dyskinesias, dystonias, and psychosis was observed. Adverse events were more frequent in bromocriptine-treated patients. Most patients and physicians preferred pergolide to bromocriptine. Pergolide as adjunctive therapy to levodopa was more effective than bromocriptine in this short-term trial.

Aged↗
PubMed1993

Long-term treatment of acromegalic patients with repeatable parenteral depot-bromocriptine.

We studied the efficacy and tolerability of a repeatable long-acting parenteral depot-bromocriptine preparation (Parlodel LAR) in 14 acromegalic patients, 10 of whom had received oral bromocriptine therapy previously, 2 of them showing intolerance to oral bromocriptine. Patients received i.m. injections of 50-100 mg depot-bromocriptine at 4-week intervals for 3-24 months (median 6). Growth hormone profiles were assessed by four daily samples at 4-week intervals. Main daily growth hormone levels decreased from 52.1 +/- 12.3 micrograms/l (mean +/- SEM) to 19.4 +/- 4.7 micrograms/l on the day of injection. In 6 patients, growth hormone values were lowered by more than 50%, whereas IGF-I levels decreased only slightly and growth hormone values during the oral glucose tolerance test remained non-suppressible. Tumour sizes were not affected. Two women became pregnant and were delivered of healthy babies. Side-effects typical of bromocriptine occurred frequently on the days of injection and diminished in most patients after 2 months of therapy despite increasing dosage. Compared with previous oral bromocriptine therapy, 9 of 10 patients preferred the depot preparation, whereas the reduction of growth hormone levels was similar during both treatments. In conclusion, depot-bromocriptine should be considered for acromegalic patients intolerant to oral bromocriptine.

Acromegaly↗
PubMed1982

Adjuvant treatment of Parkinson's disease with dopamine agonists: open trial with bromocriptine and CU 32-085.

Bromocriptine (CB-154) and the 8-alpha-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5-75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1-60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of "total disability score' at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and "on-off' effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effect including mental changes (for with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and "on-off' effects than bromocriptine.

Aged↗
PubMed1981

[Bromocriptine in patients with idiopathic edema (author's transl)].

The diuretic therapy of patients with idiopathic edema is known to induce a secondary aldosteronism, which perpetuates edema formation and exacerbates the clinical symptoms. The observation of a decreased excretion of dopamine in these patients suggests that a treatment with the orally active dopamine agonist bromocriptine might be beneficial. Nine patients with typical symptoms of idiopathic edema, which had been present for several years, were treated with bromocriptine (Pravidel) 2 X 2.5 mg/die. The response to therapy was assessed clinically by the normalization of diurnal weight gain and general well-being. Seven patients showed a good response to bromocriptine, in one patient the response was only modest, and in one patient the medication had to be stopped because of nausea. Bromocriptine normalized diurnal weight gain without inducing weight loss. Both without therapy and during bromocriptine treatment electrolytes in serum, blood pressure, plasma renin activity and aldosterone are within the normal range. From the present pilot study it can be concluded that bromocriptine is an effective alternative to the traditional diuretic therapy in some patients with idiopathic edema. It remains unclear, whether the beneficial effect of bromocriptine reveals a dopamine deficiency, or whether bromocriptine is only a symptomatic treatment.

Adult↗
PubMed2003

Ropinirole as an adjunct to levodopa in the treatment of Parkinson's disease: a 16-week bromocriptine controlled study.

BACKGROUND: and objectives Ropinirole is a non-ergoline, selective dopamine D(2) agonist. The aim of this study was to evaluate the efficacy and safety of ropinirole as an adjunct to levodopa in the treatment of Parkinson's disease (PD) complicated by motor fluctuations. METHODS: A total of 76 patients with PD (Hoehn and Yahr stage II to IV) were included in this trial. Each patient was randomly allocated to receive either ropinirole (n = 37) or bromocriptine (n = 39) as an adjunct to levodopa over a 16-week period. Ropinirole and bromocriptine were titrated for optimal efficacy and tolerability. This optimal dose was then maintained for the rest of the study. Response rate was defined as the percentage of patients who achieved at least a 20 % reduction in levodopa dose. Clinical status was also assessed using the Unified Parkinson's Disease Rating Scale (UPDRS), Clinical Global Impression (CGI), and reduction in time spent 'off'. RESULTS: Ropinirole produced a significantly greater response rate than bromocriptine (odds ratio 2.995, 95 % C. I. (1.157, 7.751) p < 0.05). There was also a statistically significant difference between the groups in the proportion of patients who were 'improved' on the CGI improvement scale (91.9 % for ropinirole, 74.3 % for bromocriptine, p = 0.046). Other measures, including at least a 20 % improvement in the UPDRS motor score (70 % for ropinirole and 63.3 % for bromocriptine), and a 20 % reduction in 'off' duration (81 % for ropinirole and 52.4 % for bromocriptine) showed a trend in favour of ropinirole. There was no significant difference between the two groups in the overall incidence of adverse effects (ropinirole, 59.5 %; bromocriptine, 59 %). In each group, the most common side-effects were dizziness, dyskinesia and nausea/vomiting. No patients were withdrawn from the study because of side-effects. CONCLUSION: Ropinirole was found to be safe and well-tolerated. Ropinirole as an adjunct to levodopa in the treatment of PD with motor fluctuation was associated with more significant reduction of levodopa dose and, on one form of analysis, with significantly greater improvement in CGI ratings than bromocriptine. On the other efficacy measures the two drugs were comparable.

Antiparkinson Agents↗
PubMed1985

The effects of chronic bromocriptine treatment on behaviour and dopamine receptor binding in the rat striatum.

Agonist-induced rotation and striatal binding of [3H]spiperone ([3H]SPIP) were assessed in rats with unilateral lesions of the substantia nigra during and after a period of chronic bromocriptine administration. Agonist-induced rotation significantly increased over a three week period of daily administration of bromocriptine (10 mg/kg i.p.); control animals were tested for agonist-induced rotation at one week intervals, which remained constant. Rotation was increased by chronic bromocriptine administration in response to either of two DA agonists, apomorphine (APO) and bromocriptine, suggesting that increased agonist sensitivity did not reflect a reduction in the metabolism of bromocriptine. Striatal binding of the dopamine D2 radioligand, [3H]SPIP, was significantly increased in the denervated striata of nigra-lesioned rats. Chronic bromocriptine administration decreased binding in denervated striata to levels not significantly different from control values. [3H]SPIP binding in intact striata was significantly reduced by bromocriptine to below control values. Differences in receptor levels reflected changes in the maximum density of binding sites with no change in affinities. Paradoxical behavioural hypersensitivity developing during chronic bromocriptine levels is not apparently mediated by changes in striatal D2 binding sites.

Animals↗
PubMed1991

Bromocriptine inhibits the seasonally occurring obesity, hyperinsulinemia, insulin resistance, and impaired glucose tolerance in the Syrian hamster, Mesocricetus auratus.

Seasonally obese-hyperinsulinemic female Syrian hamsters were injected daily with bromocriptine or saline for a period of 34 days to test for effects of bromocriptine on body fat store levels, hepatic triglyceride secretion, glucose tolerance, and plasma insulin and glucose concentrations. The effects of bromocriptine on body fat store levels, as well as on plasma insulin and glucose concentrations, in seasonally obese hamsters were compared with the levels of body fat, plasma insulin, and plasma glucose observed in seasonally lean hamsters. Bromocriptine treatment substantially improved glucose intolerance and reduced the total and stimulated areas under the glucose tolerance curve by 33% after 14 days of treatment. After 34 days of treatment, bromocriptine reduced body fat store levels by 36% and hepatic triglyceride secretion by 40% without any concurrent change in food consumption. Furthermore, bromocriptine reduced the plasma insulin level by 70%, while slightly reducing plasma glucose concentration (ie, 68% reduction in the insulin to glucose ratio). The reductions of body fat, plasma insulin, and plasma insulin to glucose ratio produced by bromocriptine in seasonally obese hamsters are equivalent to those observed in seasonally lean hamsters. Shifts in phase relationships of circadian neuroendocrine rhythms have been demonstrated to regulate annual cycles of metabolism in vertebrates, including the Syrian hamster. The effects of bromocriptine can also be explained as an alteration of such a circadian mechanism.

Adipose Tissue↗
PubMed1989

Bromocriptine antagonizes behavioral effects of cocaine in the rat.

Rats given cocaine or bromocriptine under conditions of low basal arousal showed dose-dependent increases of locomotor activity for less than or equal to 1 hours, followed by depression of activity that diminished gradually over the next 2 hours. Arousal was related biphasically to dose (maximum at ca. 5 mg/kg) but depression increased monophasically with the dose of either agent. Both behavioral arousal and depression induced by cocaine were antagonized by bromocriptine, even at doses lacking behavioral effects alone (ID50 = 1.0 and 0.36 mg/kg [1.3 and 0.5 mumol/kg], respectively). Bromocriptine blocked depression of locomotion even when given after the initial stimulation by cocaine. Bromocriptine induced very weak stereotypy, and neither increased nor blocked stereotypy induced by cocaine or apomorphine. Cocaine, at maximally effective doses, did not deplete catecholamines or serotonin in brain regions at times of maximum behavioral arousal or depression, nor did bromocriptine after metabolic turnover of dopamine. Bromocriptine antagonized arousal induced by direct injection of dopamine into the nucleus accumbens. The ability of bromocriptine to block both the behavioral arousal and depression induced by cocaine may reflect activity of bromocriptine as a mixed agonist-antagonist with limited intrinsic agonistic activity at central dopaminergic D2 receptors, perhaps with particular reference to limbic mechanisms.

Animals↗