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PubMed2000

Pergolide versus bromocriptine for levodopa-induced motor complications in Parkinson's disease.

OBJECTIVES: To compare the efficacy and safety of adjunct pergolide therapy versus bromocriptine in patients with Parkinson's disease, already established on levodopa and suffering the long-term complications of therapy. SEARCH STRATEGY: Electronic searches of MEDLINE, EMBASE and the Cochrane Controlled Trials Register. Handsearching of the neurology literature as part of the Cochrane Movement Disorders Group's strategy. Examination of the reference lists of identified studies and other reviews. Contact with Eli Lilly Company and Sandoz Limited. SELECTION CRITERIA: Randomised controlled trials of pergolide versus bromocriptine in patients with a clinical diagnosis of idiopathic Parkinson's disease and long-term complications of levodopa therapy. DATA COLLECTION AND ANALYSIS: Data was abstracted independently by each author and differences settled by discussion. MAIN RESULTS: Three short-term trials fulfilled the inclusion criteria for the review. Pergolide was superior to bromocriptine regarding UPDRS and NYPDS motor and NYPDS ADL scores in two trials. More patients recorded a 'marked' or 'moderate improvement' in clinician's global impression score with pergolide than bromocriptine in two studies. Insufficient evidence on fluctuations and dyskinesia was available to draw any conclusions. No significant differences between the agonists were seen in levodopa dose reduction, drop outs or adverse events. REVIEWER'S CONCLUSIONS: Although pergolide is superior to bromocriptine in reducing motor impairments and disability, no firm conclusions regarding levodopa-induced motor complications can be reached. Levodopa dose reduction, adverse events and withdrawals from treatment are similar for the two agonists. The small advantage of pergolide in efficacy does not take into account its additional cost compared with bromocriptine.

Antiparkinson Agents↗
PubMed2000

Lisuride versus bromocriptine for levodopa-induced complications in Parkinson's disease.

OBJECTIVES: To compare the efficacy and safety of adjunct lisuride therapy versus bromocriptine in patients with Parkinson's disease, already established on levodopa and suffering the long-term complications of therapy. SEARCH STRATEGY: Electronic searches of MEDLINE, EMBASE and the Cochrane Controlled Trials Register. Handsearching of the neurology literature as part of the Cochrane Movement Disorders Group's strategy. Examination of the reference lists of identified studies and other reviews. Contact with Cambridge Laboratories, Roche Products Limited and Sandoz Limited. SELECTION CRITERIA: Randomised controlled trials of lisuride versus bromocriptine in patients with a clinical diagnosis of idiopathic Parkinson's disease and long-term complications of levodopa therapy. DATA COLLECTION AND ANALYSIS: Data was abstracted independently by each author and differences settled by discussion. MAIN RESULTS: Only one randomised cross-over trial including 20 patients has compared lisuride with bromocriptine as adjunct therapy in Parkinson's disease. Both lisuride and bromocriptine improved motor fluctuations with no significant differences between the agonists. However, this conclusion is based on an unvalidated 4 point rating scale which could only record positive outcomes. This, combined with the small size of the trial, suggests that firm conclusions on motor fluctuations should not be drawn. Lisuride and bromocriptine produced similar benefits in parkinsonian impairments according to the Columbia Rating Scale. Adverse events were similar with the two agonists and no withdrawals were reported from either drug. REVIEWER'S CONCLUSIONS: The small size of this study and other methodological problems do not allow any firm conclusions to be drawn regarding the efficacy and safety of lisuride compared with bromocriptine in advanced Parkinson's disease with motor complications.

Antiparkinson Agents↗
PubMed2000

Pramipexole versus bromocriptine for levodopa-induced complications in Parkinson's disease.

OBJECTIVES: To compare the efficacy and safety of adjuvant pramipexole versus bromocriptine therapy in patients with Parkinson's disease, already established on levodopa and suffering from motor complications. SEARCH STRATEGY: Electronic searches of MEDLINE, EMBASE and the Cochrane Controlled Trials Register. Handsearching of the neurology literature as part of the Cochrane Movement Disorders Group's strategy. Examination of the reference lists of identified studies and other reviews. Contact with Pharmacia Upjohn and Boehringer Ingelheim. SELECTION CRITERIA: Randomised controlled trials of pramipexole versus bromocriptine in patients with a clinical diagnosis of idiopathic Parkinson's disease and long-term complications of levodopa therapy. DATA COLLECTION AND ANALYSIS: Data was abstracted independently by the authors and differences settled by discussion. The outcome measures used included Parkinson's disease rating scales, levodopa dosage, 'off' time measurements and the frequency of drop outs and adverse events. MAIN RESULTS: One randomised controlled trial has compared pramipexole with bromocriptine using a double-blind, parallel group, multicentre design. It was not powered to examine differences between active treatment arms. There was a larger reduction in off time with pramipexole therapy compared with bromocriptine (weighted mean difference 1.4 hours; 0, 2.8, 95% CI). No differences occurred in dyskinesia rating scale, dyskinesia as an adverse event or UPDRS complication score. The UPDRS ADL and motor scores showed similar improvements compared to placebo with both agonists. Levodopa dose reduction was similar with both agonists. Subscales of the Functional Status Questionnaire showed significant improvements compared to placebo with both agonists. The finding that the EuroQol improved significantly compared with placebo with pramipexole but not bromocriptine should be treated with caution. Dopaminergic adverse events were similar with each agonist, as was the all cause withdrawal rate. REVIEWER'S CONCLUSIONS: Although pramipexole and bromocriptine improved off time and reduced parkinsonian motor impairments and disability compared with placebo, no conclusions regarding their comparative effectiveness and safety can be drawn as this single trial did not have adequate power to assess such differences. Further larger trials are required to examine this issue in the future.

Antiparkinson Agents↗
PubMed1983

Bromocriptine and lisuride in Parkinson disease.

Lisuride was compared with bromocriptine in 25 parkinsonian patients in whom the response to levodopa had diminished; 19 had "wearing off," "on-off" phenomena, or both. At the time bromocriptine was added to levodopa, the mean age of the patients was 62.7 years and mean disease duration was 8.9 years. Disability decreased by 34% in the on period and by 20% in the off period, and the number of hours the patients were on increased from 9.6 to 12.8. All these changes were significant (p less than or equal to 0.01 to 0.05). Bromocriptine, however, had to be discontinued in 11 patients because of adverse effects. In the remaining 14 patients, bromocriptine was eventually discontinued because of decreased efficacy. Mean dose of bromocriptine was 55 mg (range, 20 to 100 mg). At the time lisuride was added to levodopa the patients were older (65.4 years), had had the disease longer (11.4 years), and were more disabled. Nonetheless, disability decreased in the on period by 33% and in the off period by 17%, and the number of hours the patients were on increased from 3.9 to 8.9. All these changes were significant (p less than or equal to 0.01 to 0.05). The mean dose of lisuride was 2.8 mg (range, 0.6 to 5.0 mg). Lisuride was discontinued in 8 patients because of adverse effects. Both bromocriptine and lisuride are useful in managing patients with advanced Parkinson disease whose response to levodopa has diminished. While it is presently not possible to state which of the drugs is more effective, ultimately their usage will probably be determined by their relative cost.

Aged↗
PubMed1991

The role of prolactin in autoimmune demyelination: suppression of experimental allergic encephalomyelitis by bromocriptine.

Several lines of evidence suggest that the anterior pituitary hormone prolactin has a stimulatory role on immune function and that pharmacological suppression of prolactin secretion with the dopamine-agonist bromocriptine suppresses both humoral and cellular immunity. Here, we describe the effects of prolactin-suppression on the course of experimental allergic encephalomyelitis in female Lewis rats. Initiation of continuous bromocriptine treatment before immunization reduced both the severity and incidence of clinical signs of acute experimental allergic encephalomyelitis. Experimental allergic encephalomyelitis-immunized rats experienced a threefold rise in basal prolactin levels on day 4 after immunization and maintained elevated prolactin levels on day 10, before the onset of neurological signs of experimental allergic encephalomyelitis. Bromocriptine treatment reduced prolactin levels to those of sham-immunized rats. In vivo bromocriptine pretreatment inhibited splenic lymphocyte proliferative responses in vitro to the immunizing antigen and to concanavalin A. Moreover, bromocriptine therapy was protective when initiated 1 week after the initial immunization and was also effective in suppression of late disease. These results indicate that (1) prolactin levels are elevated after immunization and before the onset of experimental allergic encephalomyelitis, (2) bromocriptine inhibits both prolactin secretion and the severity of acute experimental allergic encephalomyelitis, and (3) inhibition is also present when treatment is begun after sensitization, suggesting an effect of prolactin on the effector limb of the immune response during experimental allergic encephalomyelitis.

Animals↗
PubMed1999

Effect of bromocriptine on uterine contractility in near-term pregnant rats.

Treatment of pregnant albino rats at gestation day 9 with the dopamine agonist, bromocriptine, in a dose of 0.7 mg kg-1 day-1, i.p. for 11 days produced a significant increase in the normal uterine contractions both in vitro and in vivo. The increase in frequency (F), amplitude (A) and area under the curve (AUC) in the in vitro experiment amounted to 35, 80 and 58%, respectively; while the increase in F and A in the in vivo experiment was 36 and 25%, respectively, in comparison with the corresponding control group. Addition of oxytocin (5x10(-12)-4x10(-11) m) to the uterus isolated from rats pretreated with bromocriptine resulted in marked uterotonic effect (24, 35 and 49% increase in F; 25, 35 and 46% increase in A and 42, 62 and 122% increase in AUC of contractions). Also, the in vivo experiment showed that an injection of oxytocin at the time of investigation (0.125-1.0 I.U. kg-1, i.v.) into rats pretreated with bromocriptine caused a marked increase in F (33, 40 and 81%) and A (33, 37 and 75%) of uterine contractions compared to the values of bromocriptine-treated animals. These results indicate that bromocriptine should be used with caution during pregnancy. In addition, this must be considered when using oxytocin during delivery of females pretreated with bromocriptine.

Animals↗
PubMed1986

Bromocriptine in the treatment of hypertension.

The efficacy of bromocriptine in the treatment of hypertension was assessed in a double-blind placebo controlled cross-over study preceded by a dose titration phase. A diuretic and/or a beta-blocker were administered concomitantly in constant dosage to 11 of the 20 patients who received bromocriptine. A wide range of doses of bromocriptine was tolerated. Side-effects of vomiting and postural hypertension did not occur, possibly due to the gradual increase in the administered doses. Plasma prolactin was not raised in this population of hypertensives. In the dose titration phase (n = 20), a small fall in diastolic but not in systolic blood pressure occurred with bromocriptine, but only with the patient standing and after exercise. In the double-blind phase (n = 9), there was no significant difference in blood pressure between the bromocriptine and placebo treatments. It is concluded that bromocriptine was not effective in lowering blood pressure in the present patients with essential hypertension.

Adult↗
PubMed1987

Differential action of bromocriptine on nigrostriatal versus mesolimbic dopaminergic neurons.

The present study was undertaken to compare the abilities of the dopaminergic agonists apomorphine, bromocriptine, and lergotrile to inhibit the synthesis of dopamine (DA) in terminals of nigrostriatal and mesolimbic DA neurons. The in vivo synthesis of DA was estimated by measuring the rate of accumulation of dihydroxyphenylalanine (DOPA) in terminals of nigrostriatal (striatum) and mesolimbic (nucleus accumbens, olfactory tubercle) neurons 30 min after the administration of NSD 1015, a decarboxylase inhibitor. The activation of DA autoreceptors in these regions was evaluated by measuring the abilities of the DA agonists to inhibit DA synthesis in brain regions of rats pretreated with gamma-butyrolactone (GBL). Apomorphine (0.03-1.0 mg/kg for 45 min) and bromocriptine (0.1-10 mg/kg for 90 min) produced dose-dependent decreases in the rate of DA synthesis in all three brain regions of both vehicle- and GBL-treated rats. A time course of the effects of the highest dose of bromocriptine (10 mg/kg), however, demonstrated dramatic regional differences in the ability of this drug to inhibit DA synthesis in saline-versus GBL-pretreated rats. Bromocriptine inhibited the GBL-induced increase in DA synthesis for 6 hours in all regions examined. In the striatum of saline-treated rats the decrease in DA synthesis was evident only at 1.5 hours after bromocriptine administration, while in the nucleus accumbens and olfactory tubercle DA synthesis remained inhibited for 6 hours. By contrast, lergotrile reduced DA synthesis to a similar extent in all three regions for at least 6 hours in both vehicle- and GBL-treated rats. These results suggest that there is no regional difference in the ability of bromocriptine to inhibit DA synthesis via DA autoreceptor mechanisms, but there appear to be differences in postsynaptic DA receptor-mediated mechanisms which regulate nigrostriatal versus mesolimbic DA neurons.

4-Butyrolactone↗
PubMed2002

Inhibitory mechanism of bromocriptine on catecholamine release evoked by cholinergic stimulation and membrane depolarization from the rat adrenal medulla.

The purpose of this study was to determine whether bromocriptine affects the catecholamines (CA) secretion evoked in isolated perfused rat adrenal glands, by cholinergic stimulation, membrane depolarization and calcium mobilization, and to establish the mechanism of its action. The perfusion of bromocriptine (1-10 microM) into an adrenal vein, for 60 min, produced relatively dose-dependent inhibition in the secretion of catecholamines (CA) evoked by acetylcholine (ACh, 5.32 mM), DMPP (100 microM for 2 min), McN-A-343 (100 microM for 2 min), cyclopiazonic acid (CPA, 10 microM for 4 min) and Bay-K-8644 (10 microM for 4 min). High K+ (56 mM)-evoked CA release was also inhibited, although not in a dose-dependent fashion. Also, in the presence of apomorphine (100 microM), which is also known to be a selective D2-agonist, the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly depressed. However, in adrenal glands preloaded with bromocriptine (3 microM) in the presence of metoclopramide (15 microM), a selective D2-antagonist, the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid considerably recovered as compared to that of bromocriptine only. Taken together, these results suggest that bromocriptine can inhibit the CA secretion evoked by stimulation of cholinergic receptors, as well as by membrane depolarization, in the perfused rat adrenal medulla. It is thought this inhibitory effect of bromocriptine may be mediated by inhibiting the influx of extracellular calcium and the release from intracellular calcium stores, through the activation of dopaminergic D2-receptors located in the rat adrenomedullary chromaffin cells. Furthermore, these findings also suggest that the dopaminergic D2-receptors may play an important role in regulating adrenomedullary CA secretion.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed2006

Dopamine D2 agonists, bromocriptine and quinpirole, increase MPP+ -induced toxicity in PC12 cells.

Dopaminergic cell loss in the mesencephalic substantia nigra is the hallmark of Parkinson's disease and may be associated with abnormal oxidative metabolic activity. However, the delicate balance underlying dopamine decline and oxidative stress is still a matter of debate. The aim of this study was to analyze the possible modulation of D2 agonists and antagonists on MPP+ (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinium ion) -induced cellular death in differentiated and undifferentiated PC12 cells. Using colorimetric assays, western blots and reverse transcriptase-PCR, we demonstrated that two D2 agonists, bromocriptine and quinpirole, consistently increased MPP+ -induced cytotoxicity in both differentiated and undifferentiated PC12 cells, whereas D2 antagonists do not modulate cell death. However, this increase in cellular death was reversed when bromocriptine or quinpirole were used in presence of D2 antagonists. On the other hand, 1-{2-[bis-(4-fluorophenyl)methoxy]ethyl}-4-(3-phenylpropyl)piperazine (GBR 12909), a potent inhibitor of the dopamine transporter, partially reversed MPP+ -induced cellular death and completely abolished the increase of cellular death induced by bromocriptine. Dopamine agonists and antagonists also modulate the expression of the dopamine transporter in PC12 cells; in particular, bromocriptine may alter MPP+ uptake by increasing DAT expression We also show that, in our cellular paradigm, D2 receptor mRNA levels are more abundant that D3 mRNA levels and MPP+ and /or bromocriptine could not modulate D2 gene expression while D3 gene expression clearly decrease after MPP+ and /or bromocriptine treatment.

1-Methyl-4-phenylpyridinium↗
PubMedDate not supplied

Microdialysis study of bromocriptine and its metabolites in rat pituitary and striatum.

Bromocriptine, a D2 receptor agonist, was administered intravenously (1mg/kg) to anesthetized rats. Microdialysis probes were implanted in the pituitary and the striatum, known sites of D2 agonist action. Bromocriptine and its metabolites were monitored in plasma and tissue dialysates for 4 h. Drug analyses were performed using two different enzyme immunoassays specific for untransformed bromocriptine or a pool of parent drug plus hydroxylated metabolites. The metabolites/parent drug ratio for areas under the curve was 5.5 in plasma and 1 in the pituitary. No metabolites could be detected in the striatum. Bromocriptine penetration was at least 10-fold greater in the pituitary than in the striatum. The kinetics of bromocriptine in the pituitary and striatum did not parallel those in plasma, indicating that the prolonged action of bromocriptine reported by other authors may be due to slow dissociation from receptors.

Animals↗
PubMedDate not supplied

Nasal spray vs oral administration of bromocriptine: pharmacology and effect on serum prolactin in puerperal women.

The oral administration of bromocriptine induces a variety of side-effects in about 50-70% of patients, the most common being nausea and vomiting, probably related to the local gastrointestinal effect of the drug. Nasal administration makes it possible to avoid intestinal and liver metabolism. This study compared the serum concentrations of bromocriptine and prolactin (PRL) in twenty puerperal women who had asked to discontinue breast feeding and were randomized to receive a single oral (2.5 mg) or nasal spray dose (0.8 mg) of bromocriptine. Serum bromocriptine and PRL concentrations were measured at various times before and after drug administration. At 15 min, the circulating concentrations of bromocriptine were about eight times higher after nasal than after oral administration; peak serum concentration (CMax) was reached respectively 45 min and 60 min after administration, and was about three times higher after nasal administration (314 +/- 102 pg/ml vs 112.30 +/- 34.47 pg/ml). The reduction in serum PRL concentrations was also more rapid in the nasally-treated group reaching the normal assay range of < 20 micrograms/l within two as against five hours post-administration. Four orally-treated patients complained of nausea; in the nasally-treated group, six patients reported only a mild endonasal burning that disappeared within a few minutes of administration. Our results suggest that the nasal administration of bromocriptine may lead to a reduction in the required overall dose and fewer gastrointestinal side-effects, and may therefore improve therapy compliance.

Administration, Intranasal↗
PubMed1986

Chronic treatment with L-DOPA, but not bromocriptine induces dyskinesia in MPTP-parkinsonian monkeys. Correlation with [3H]spiperone binding.

A group of 5 monkeys developed a severe parkinsonian syndrome after intravenous administration of the toxin MPTP. One remained untreated while two animals were treated daily for 5 months with supramaximal doses of Sinemet and two with bromocriptine orally. Both drugs relieved the parkinsonian symptoms but the animals on Sinemet developed after 2 weeks prominent lingual dyskinesia which remained visible after each dose until the end of the experiment. In the two animals on bromocriptine no dyskinesia was observed. After sacrifice, the levels of dopamine and [3H]spiperone binding were studied bilaterally in the anterior and posterior caudate nucleus, anterior and posterior putamen and in the nucleus accumbens. The loss of dopamine was equivalent in the Sinemet and the bromocriptine treated animals (more than 90%) and there was a complete disappearance of the substantia nigra pars compacta. In all structures studied, the Bmax for [3H]spiperone binding was on average 10% higher in the Sinemet than in the bromocriptine-treated animals. We therefore believe that L-DOPA and bromocriptine affect denervated postsynaptic dopamine receptors differently, that bromocriptine is less likely to induce agonist supersensitivity and that this probably explains the lesser tendency to induce dyskinesia after chronic treatment.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1988

Repeated stimulation of D-1 dopamine receptors increases the circling response to bromocriptine in rats with a 6-OHDA lesion.

We have studied the effect of repeated injections of a specific D-1 agonist, (SKF 38393), on circling behaviour in response to a specific D-2 agonist (bromocriptine) and on striatal D-2 DA receptors in rats with a unilateral lesion of the nigrostriatal pathway. Two groups of rats were formed on the basis of their circling response to a first injection of SKF 38393: clear contralateral circling (SKF-positive) and no (or ipsiversive) circling (SKF-negative). A few days later, these rats were tested once for bromocriptine-induced circling. A repeated treatment of 8 injections of SKF 38393 over 4 days was started the next day. The animals were tested again for bromocriptine-induced circling at the end of the repeated treatment with the D-1 agonist. A third group of rats received only the 2 test injections of bromocriptine and a fourth group included intact control animals. During the repeated treatment, the D-1 agonist induced an increase of the circling response up to the fourth injection and a decrease thereafter in the SKF-positive group. This was followed by a pronounced increase of circling in response to the second injection of bromocriptine. This increased sensitivity appears to be due to the chronic treatment with SKF 38393 since animals that did not respond initially to the D-1 agonist (SKF-negative group) and those that received only 2 injections of bromocriptine showed no increase of their circling response. The treatments did not increase the affinity of [3H]spiperone binding for the striatal D-2 dopamine receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1986

Rapid regression through bromocriptine therapy of a suprasellar extending prolactinoma during pregnancy.

A 29-year-old woman is described who presented with amenorrhea and galactorrhea with a large prolactinoma which regressed on bromocriptine therapy. Treatment with bromocriptine was stopped when pregnancy was diagnosed but 6 weeks later the prolactinoma had regrown with suprasellar extension and lateral invasion of the cavernous sinus. When treatment with bromocriptine was reinstituted symptoms subsided within 24 h and serum prolactin concentrations fell from 54,000 mM/l to 2800 mU/l within 5 days and 500 mU/l 2 days after that. Pregnancy proceeded without complications and she entered spontaneous labor at term and delivered a healthy baby. One year after delivery, on treatment with bromocriptine, her serum prolactin concentration remains within the normal range and the CT scan shows persistence of a small prolactinoma, confined to the pituitary fossa. Bromocriptine should be the primary treatment for prolactinomas regardless of tumor size and may be safely stopped when pregnancy is desired. If pituitary tumor complications occur during pregnancy, reintroduction of treatment with bromocriptine should again be the treatment of choice.

Adult↗
PubMed1995

Bromocriptine protects against delayed neuronal death of hippocampal neurons following cerebral ischemia in the gerbil.

Bromocriptine, a dopamine D2 receptor agonist, has widely been used for patients with Parkinson's disease. In this study, we examined its neuroprotective effects against neuronal damage in the CA1 subfield of the hippocampus following experimental cerebral ischemia in the Mongolian gerbil. Forebrain ischemia was induced by occlusion of bilateral common carotid arteries for 3 min. Bromocriptine, at a dose of 0.3 or 3 mg/kg, was injected i.p. 30 min before the onset of ischemia. Histopathological observations showed that neuronal damage to hippocampal CA1 neurons, which was seen 7 days after ischemia in vehicle-treated animals, was prevented by bromocriptine treatment. Immunohistochemical staining for copper/zinc superoxide dismutase and manganese superoxide dismutase decreased markedly in the CA1 neurons of vehicle-treated animals 2 days after ischemia when histological neuronal destruction was not yet seen, but was well preserved in bromocriptine-treated animals. The present findings show that bromocriptine protects against ischemia-induced neuronal damage, and that the mechanism of the neuroprotection may relate to the preservation of SODs. Bromocriptine, which was recently shown to be a potent free radical scavenger, may have a potent neuroprotective action against disorders including ischemic stroke.

Animals↗
PubMed1995

Bromocriptine inhibits in vivo free fatty acid oxidation and hepatic glucose output in seasonally obese hamsters (Mesocricetus auratus).

Seasonally obese hyperinsulinemic hamsters were treated for 5 weeks with bromocriptine (500 to 600 micrograms per animal) and tested for drug effects on energy balance, body fat stores, nocturnal whole-body free fatty acid (FFA) metabolism and hepatic glucose output, and diurnal glucose tolerance. After 5 weeks, bromocriptine treatment reduced retroperitoneal fat pad weight by 45% without altering either daily food consumption or end-treatment total daily energy expenditure. Also, 5 weeks of treatment improved the diurnal glucose tolerance, resulting in a 47% and 33% decrease in the area under glucose and insulin curves, respectively. After 4 weeks, bromocriptine treatment reduced nocturnal lipolysis by 28%, palmitate rate of appearance into plasma by 30%, palmitate oxidation by 33%, and hepatic glucose output by 28%. Moreover, these reductions were accompanied by a 75% reduction in plasma insulin concentration. The data suggest that bromocriptine may improve diurnal glucose tolerance in part by inhibiting the preceding nocturnal lipolysis and FFA oxidation. Reductions in nocturnal FFA oxidation and hepatic glucose production may result from bromocriptine's influences on circadian organization of hypothalamic centers known to regulate these activities. Available evidence suggests that bromocriptine may impact this neuroendocrine organization of metabolism by increasing the dopamine to noradrenaline activity ratio in central (hypothalamic) and peripheral (eg, liver and adipose) target tissues.

Animals↗
PubMed1987

Behavioral and biochemical evidence for a different effect of repeated administration of L-dopa and bromocriptine on denervated versus non-denervated striatal dopamine receptors.

The effect of repeated administration of bromocriptine and L-3,4-dihydroxyphenylalanine (L-DOPA) was studied behaviorally and biochemically in rats with a unilateral lesion of the nigrostriatal pathway. Groups of rats injected eight times with bromocriptine or L-DOPA significantly increased their contraversive circling. Rats receiving only two injections of bromocriptine did not. Animals receiving two injections of L-DOPA showed a slight but significant increase in circling. The affinity of the binding of [3H]spiperone to the dopamine receptors was unchanged by the lesion or the treatments, while the density of the binding was significantly modified. Chronic treatment with bromocriptine induced a significant decrease in the density of D2 dopamine receptors in the intact striata, while on the lesioned side, it remained unchanged. By contrast, chronic administration of L-DOPA induced a significant increase in density of the striatal dopamine receptors in the lesioned striata in addition to that caused by denervation, while the decrease on the intact side was not significant. It seems that contrary to the intact striatum, the lesioned side had a defective down-regulation mechanism in response to chronic treatment with a dopamine agonist. The results also show that L-DOPA was more potent than bromocriptine in inducing agonist supersensitivity in a denervated striatum. This may explain why chronic treatment with bromocriptine has a lesser tendency to induce dyskinesia in patients with Parkinson's disease.

Animals↗