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At least 19 recordsLinked to original sources
PubMed1983

Microbial transformations of pergolide to pergolide sulfoxide and pergolide sulfone.

Fifty-eight microorganisms were investigated for their ability to effect the biotransformation of the ergoline alkaloid pergolide. A majority of these organisms formed pergolide sulfoxide, and a Helminthosporium species was investigated in greater detail since it yielded significant amounts of pergolide sulfoxide. A preparative-scale transformation afforded material which was identified as the sulfoxide based on melting point, spectral, and chromatographic comparison with authentic material as well as its conversion to pergolide by reduction with triphenylphosphine. An analytical high-performance liquid chromatographic determination of the enzymatic versus spontaneous air-oxidation of pergolide in growing cultures and controls showed negligible air-oxidation and an approximately 40% enzymatic conversion of pergolide to the sulfoxide. Several organisms, including Aspergillus alliaceus formed a second metabolite, pergolide sulfone, which was identified on the basis of co-chromatographic data.

Aspergillus↗
PubMed1981

Repeated administration of pergolide to rats attenuates the acute elevation of serum corticosterone by pergolide.

A single injection (0.3 mg/kg IP) of pergolide mesylate, a dopamine agonist, increased serum corticosterone concentration several-fold in rats. This increase did not occur or was greatly diminished in rats that had received four previous daily injections of pergolide. The non-responsiveness to pergolide persisted at the second day after the last of 4 daily injections of pergolide, but by the third and fourth days the rats were again responsive to pergolide in terms of serum corticosterone elevation. The lowering of dopamine metabolites (3,4-dihydroxyphenylacetic acid and homovanillic acid) by pergolide occurred in pergolide-pretreated rats to the same extent as in control rats. Serum corticosterone concentration in pergolide-pretreated rats was elevated normally by a serotonin agonist, quipazine. Since the pituitary-adrenocortical system can be activated in pergolide-pretreated rats (indicated by the normal response to quipazine), the insensitivity to pergolide may be due to decreased responsiveness of central dopamine receptors mediating corticosterone elevation by pergolide.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Pergolide monotherapy in the treatment of early PD: a randomized, controlled study. Pergolide Monotherapy Study Group.

OBJECTIVE: To determine whether pergolide monotherapy provides symptomatic relief in early PD. BACKGROUND: Early treatment with dopamine agonists may reduce the risk of motor fluctuations, which are most likely linked to levodopa therapy. Pergolide, a D1-D2 dopamine agonist, has been studied as "add on" therapy in PD, but no controlled clinical trial studying the efficacy of pergolide monotherapy is available. METHODS: The efficacy and tolerability of pergolide were evaluated in a multicenter, double-blind, randomized, parallel-group, 3-month trial versus placebo. Patients with a diagnosis of idiopathic PD, a modified Hoehn & Yahr score of 1 to 3, and a score greater than 14 points on the Unified Parkinson's Disease Rating Scale (UPDRS) part III at baseline were enrolled in the study (pergolide, n = 53; placebo, n = 52). RESULTS: Patient characteristics at study entry were comparable in the two study groups. The pergolide group showed a significantly greater percent of responders (defined as a -30% decrease in UPDRS part III score at end point) compared with placebo (57% versus 17%; p < 0.001). Pergolide-treated patients experienced a significantly greater improvement than placebo-treated patients (p < 0.001) in UPDRS (overall, part II, and part III) score, Schwab & England score, and Clinical Global Impression improvement score. By the study end the mean dose of pergolide was 2.06 mg/day. Six patients in the pergolide group versus two patients in the placebo group discontinued the study because of treatment emergent side effects. CONCLUSION: This study suggests that pergolide monotherapy may be an efficacious and well-tolerated first-line treatment in patients with early-stage PD.

Aged↗
PubMed1997

Pergolide: treatment of choice in restless legs syndrome (RLS) and nocturnal myoclonus syndrome (NMS). A double-blind randomized crossover trial of pergolide versus L-Dopa.

A double-blind randomized crossover study of 0.125 mg Pergolide (Lilly) at bedtime versus 250mg L-Dopa + Carbidopa (Roche) was conducted in 16-day phases in 11 patients with idiopathic restless legs syndrome. Two patients reported a partial and 9 patients a complete relieve of motor restlessness while receiving Pergolide. Only 1 patient experienced an improvement of restlessness after L-Dopa. The patients showed polysomnographically a mean decrease in NMS cluster disturbed time by 45% from control on L-Dopa (p < 0.025) and by 79% from control on Pergolide (p < 0.001). In addition, Pergolide increased the total sleep time compared to L-Dopa (p < 0.05). In conclusion, the dopamine agonist Pergolide is superior to L-Dopa in the treatment of RLS and NMS.

Aged↗
PubMed1985

Pharmacological, hemodynamic and biochemical mechanisms involved in the blood pressure lowering effects of pergolide, in normotensive and hypertensive dogs.

In pentobarbital-anesthetized normotensive dogs, clonidine (20.0 micrograms/kg i.v.), in contrast to pergolide (30.0 micrograms/kg i.v.), reduced significantly both aortic blood pressure and plasma concentration of norepinephrine. However, in dogs that had been made hypertensive by sectioning the vagi and carotid sinus nerves, pergolide, like clonidine, lowered the blood pressure and plasma concentrations of epinephrine and norepinephrine that were enhanced markedly by deafferentation. Furthermore, in this preparation pergolide decreased the calculated resistance in vascular regions supplied by the upper abdominal aorta and the innervated femoral and renal arteries, but it increased vascular resistance in the denervated hind leg. Pergolide (1.0 microgram/kg) injected intracisternally (i.c.m.) induced a fall in blood pressure of comparable magnitude to that produced by a 30 times higher i.v. dose. Intravenously and i.c.m. administered pergolide lowered blood pressure by acting at distinct anatomical sites inasmuch as i.v. sulpiride blocked the effects of i.v. but not i.c.m. pergolide. The combination of sulpiride plus yohimbine injected i.c.m. was necessary to abolish the decrease in blood pressure evoked by i.c.m. pergolide. In atropinized spinal dogs, i.v. pergolide inhibited the vasoconstriction elicited by electrical stimulation of the lumbar sympathetic chain, an effect which was antagonized by sulpiride. Similarly, pergolide (30.0 micrograms/kg i.v.) like clonidine, reduced the heart rate and coronary venous plasma norepinephrine concentration raised by sustained electrical stimulation of the cardioaccelerator nerve. Sulpiride, but not phentolamine, antagonized this pergolide-induced inhibition of sympathetic nerve function. In chlorisondamine-pretreated dogs, pergolide produced a transient pressor response due to stimulation of postsynaptic vascular alpha-2 adrenoceptors. In conclusion, the failure of i.v. pergolide to decrease aortic blood pressure in pentobarbital-anesthetized normotensive dogs is presumably due to the inability of pergolide to produce a significant inhibition of the vascular sympathetic tone in this preparation. However, in neurogenic hypertensive dogs which are characterized by an elevated level of sympathetic drive, i.v. pergolide reduced blood pressure and aortic plasma norepinephrine concentration. These effects of pergolide are compatible with a DA-2 dopamine receptor stimulation on peripheral sympathetic nerve fibers. In contrast, the antihypertensive effects of i.c.m. pergolide would appear to be mediated by both alpha-2 adrenoceptors and DA-2 dopamine receptors located within the central nervous system.

Anesthesia↗
PubMed1983

Central and peripheral dopaminergic mechanisms in the cardiovascular actions of pergolide in neurogenic hypertensive dogs.

The cardiovascular actions of the dopaminergic ergoline, pergolide were examined in pentobarbital-anesthetized dogs. When administered intravenously (i.v.) to dogs made hypertensive by sino-aortic deafferentation, pergolide produced a sustained reduction in blood pressure, dilatation of the hindlimb vasculature and bradycardia. The antihypertensive action of pergolide in neurogenic hypertensive dogs was converted into a pressor action when it was given to dogs pretreated with i.v. sulpiride or hexamethonium plus atropine. Pergolide caused significant impairment of renal vasoconstriction elicited during stimulation of renal sympathetic nerves but not that caused by exogenous norepinephrine. The inhibitory action of pergolide on renal sympathetic nerve function was antagonized by sulpiride suggesting that pergolide activated presynaptic dopamine receptors. Direct administration of pergolide within the central nervous system via the cisterna magna (i.c.) to normotensive dogs also resulted in hypotension, bradycardia and iliac vasodilatation. The central actions of pergolide were prevented by sulpiride (i.c.) but not by yohimbine (i.c.), which indicates that specific activation of central dopamine receptors was responsible for these actions of pergolide. The antihypertensive, bradycardic and iliac vasodilatory actions of i.v. pergolide in neurogenic hypertensive dogs were significantly attenuated by i.c. sulpiride. It was determined that while this dose of sulpiride antagonized central dopamine receptors, it did not antagonize peripheral presynaptic dopamine receptors. These results suggest that pergolide exerts antihypertensive and bradycardic actions via simultaneous stimulation of dopamine receptors in the brain and on postganglionic sympathetic neurons. While presynaptic dopamine receptor activation contributes to the blood pressure lowering action of pergolide, stimulation of central dopamine receptors appears to be the dominant mechanism by which pergolide elicits the observed antihypertensive and bradycardic effects. Pergolide appears to lower blood pressure by a novel mechanism of action and may offer an additional therapeutic approach for the treatment of hypertension.

Animals↗
PubMed1981

Pergolide mesylate: its effects on circulating anterior pituitary hormones in man.

Pergolide mesylate is a synthetic ergoline with dopamine agonist properties. The endocrine profile was studied in a double blind crossover design in six normal males. Circulating PRL, TSH, GH, LH, FSH, and cortisol were measured in the basal state and after TRH (500 micrograms iv) administration at 4.5, 11.5, and 23.5 h after placebo or pergolide (100 micrograms orally). Pergolide caused suppression of basal PRL from 2-8 ng/ml to less than 2 ng/ml commencing 60 min after administration and persisting throughout the 23.5-h study period. For the three TRH tests, a suppression of peak PRL (mean +/- SEM) response to TRH of 54.6 +/- 5.1 vs. 1.9 +/- 0.5, 45.2 +/- 4.1 vs. 4.5 +2- 0.6, and 34.4 +/- 2.9 vs. 6.9 +/- 1.4 ng/ml, respectively, for placebo and pergolide was noted. Basal TSH levels were unaffected by pergolide, but after pergolide the peak TSH response to the first two TRH challenges was blunted (placebo vs. pergolide: 12.3 +/- 1.2 vs. 6.8 +/- 1.0 and 14.8 +/- 2.0 vs. 9.6 +/- 1.0, respectively); however, the third TSH response (9.8 +/- 1.1 vs. 9.3 +/- 1.2) was not blunted after pergolide. GH secretion was stimulated by pergolide with a consistent pulse observed within 60 min of pergolide administration and an enhancement in the number and amplitude of subsequent GH pulses throughout the 24-h period. Cortisol levels rose after pergolide and returned to levels seen on the control day at 16.5 h. FSH levels were unaffected but LH levels were lowered pergolide. Side effects including nausea, vomiting, and hypotension were observed in all subjects. Pergolide is a potent dopamine agonist with the anticipated endocrine profile and clinical effects; its long duration of actions offers promise of single daily dose therapy for hyperprolactinemia.

Adult↗
PubMed2001

Randomized trial of tolcapone versus pergolide as add-on to levodopa therapy in Parkinson's disease patients with motor fluctuations.

In this 12-week, randomized, open-label, blinded-rater, parallel-group trial, the efficacy, safety, and tolerability of tolcapone and pergolide were compared in parkinsonian patients with a fluctuating response to levodopa. Patients received tolcapone 100 mg three times daily (t.i.d.), with a possible increase to 200 mg t.i.d., or pergolide titrated to a maximum dose of 5 mg/day by week 9 (mean final dose 2.2 mg/day). The trial involved 203 patients. Efficacy variables that decreased from baseline to week 12 with tolcapone and pergolide included "off" time (reduced by 2-3 hours/day), daily levodopa intake, sickness impact profile scores, Parkinson's disease questionnaire (PDQ)-39 scores, and Unified Parkinson's Disease Rating Scale (UPDRS) scores. Improvements in efficacy variables were similar with tolcapone and pergolide, with the exception of improvements in quality of life, which were significantly greater with tolcapone; the relative changes in PDQ-39 score at week 12 were -8.7 and -14.2 (P < 0.05) with pergolide and tolcapone, respectively. Improvements in the investigator's global assessment (IGA) of overall efficacy were recorded in 86% of tolcapone-treated patients and in 78% of pergolide-treated patients. The proportion of patients who withdrew because of adverse events was higher in the pergolide group (15%) than in the tolcapone group (5%). Confusion, hypotension, nausea, constipation, abdominal pain, and dyspepsia occurred more frequently with pergolide, whereas diarrhea and urine discoloration occurred more frequently with tolcapone. Tolcapone was better tolerated than pergolide (P < 0.01) according to the IGA of overall tolerability. We conclude that, in this 3-month study, both tolcapone and pergolide provided improvements in motor fluctuations and allowed reductions in levodopa intake when added to levodopa therapy; intent to treat analysis and a less than maximal dose of pergolide may have biased the results in favor of tolcapone. Tolcapone provided greater improvements in quality of fife, was better tolerated, and had a more favorable adverse-event profile than pergolide.

Antiparkinson Agents↗
PubMed1984

Pharmacological, hemodynamic and autonomic nervous system mechanisms responsible for the blood pressure and heart rate lowering effects of pergolide in rats.

In conscious spontaneously hypertensive rats, pergolide (50.0 micrograms/kg s.c.) produced a sustained decrease in tail artery pressure which was blocked by haloperidol (1.0 mg/kg s.c.) pretreatment. In anesthetized spontaneously hypertensive rats this effect was accompanied by a fall in total peripheral resistance inasmuch as pergolide did not significantly change cardiac output. In anesthetized normotensive rats, pergolide (30.0 micrograms/kg i.v.) also lowered blood pressure. This effect was not significantly modified by adrenalectomy, methysergide, idazoxan (alpha-2 adrenoceptor antagonist), vagotomy alone or plus ligation of carotid arteries or plus atenolol, but was entirely prevented by domperidone or sulpiride pretreatment and was reverted to a pressor response (due to stimulation of alpha adrenoceptors and 5-hydroxytryptamine receptors) by blockade of ganglionic transmission with chlorisondamine. Pergolide given either i.v. or into the cisterna magna or the lateral cerebral ventricle produced changes in blood pressure of the same magnitude. In intact or adrenalectomized rats, i.v. pergolide significantly lowered plasma norepinephrine concentration. Furthermore, in saline but not sulpiride-pretreated pithed rats, pergolide reduced the pressor responses and the accompanying increases in plasma norepinephrine evoked by electrical stimulation of the spinal cord. However, pergolide failed to modify the vascular reactivity to several pressor agents and lacked beta-2 and DA-1 dopamine receptor agonist properties. These results indicate that the decrease in blood pressure produced by pergolide can be accounted for by an inhibition of sympathetic tone resulting from stimulation of peripheral neuronal dopamine receptors. A possible central contribution remains to be substantiated. The pronounced bradycardia produced by pergolide (30.0 micrograms/kg i.v.) in anesthetized intact rats was partly reduced by vagotomy, methylatropine, domperidone, sulpiride, idazoxan, phentolamine or atenolol. The effects of pergolide in vagotomized rats were further diminished by domperidone but they were blocked by the combination of phentolamine or idazoxan plus domperidone. In rats pretreated with atenolol or in rats with the cervical section of spinal cord and the low level of heart rate increased with an isoprenaline infusion, the decrease in heart rate produced by pergolide was abolished by domperidone, methylatropine or idazoxan. In pithed rats, pergolide changed neither the base-line heart rate nor the tachycardia to exogenous norepinephrine nor the bradycardia evoked by carbachol or electrical stimulation of the peripheral cervical vagus.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenalectomy↗
PubMed2000

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

OBJECTIVES: To compare the efficacy and safety of adjunct pergolide therapy versus placebo in patients with Parkinson's disease suffering from the complications of levodopa 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 and Company Limited. SELECTION CRITERIA: Randomised controlled trials of pergolide versus placebo 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. 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: A large number of small RCTs were identified, but these were part of a large multicentre trial which was eventually published in full. The final publication was used as the only subject for this review. The time patients spent 'off' was reduced by 1.8 hours with pergolide compared with 0.2 hours with placebo (p < 0.001). Dyskinesia developed or deteriorated in 62% of pergolide-treated compared with 25% placebo-treated patients (p < 0. 05). The excess in dyskinesia prevalence and severity resolved by the end of the study with levodopa reduction. Levodopa dose was reduced more in those receiving pergolide (235 mg v 51 mg; p < 0. 001). Pergolide produced significant improvement in Hoehn and Yahr stage (p < 0.05) and both the motor and activities of daily living parts of a modified Columbia rating scale (both p < 0.001). Significantly more patients suffered nausea (24% v 13%; p < 0.001) and hallucinations (14% v 3%; p < 0.01) on pergolide. No difference was found in the numbers remaining on treatment at the end of the study (pergolide 84% v placebo 82%) but withdrawals due to adverse events were greater in those taking pergolide (10% v 4%). REVIEWER'S CONCLUSIONS: Based on this single large multicentre study, pergolide reduces 'off' time and improves impairment and disability due to Parkinson's disease whilst allowing a reduction in levodopa dose. This is at the expense of dopaminergic adverse events. Further trials are required to compare pergolide with the newer dopamine agonists.

Antiparkinson Agents↗
PubMed1985

Behavioral effects of pergolide mesylate on food intake and body weight.

In a crossover design experiment, pergolide mesylate significantly suppressed food intake and body weight in spayed female rats. Inhibition of food intake by a constant dose of pergolide progressively diminished with repeated administrations. Pergolide continued to suppress body weight with no indications of tolerance. When pergolide was discontinued, body weight increased sufficiently to compensate for the loss and failure to gain during drug treatment. A second experiment investigated the observation that animals injected first with vehicle showed greater anorexia when subsequently injected with pergolide than did animals injected first with pergolide. In addition, tolerance was further assessed by administering on two occasions a higher dose of pergolide. Following chronic pergolide treatment, this dose was insufficient to reinstate anorexia; however, after a period of abstinence, this dose produced anorexia comparable to that observed at the beginning of pergolide treatment. Due to pergolide mesylate's action as a postsynaptic dopamine agonist, a dopaminergic neural system is implicated in pergolide induced anorexia.

Animals↗
PubMed1992

Behavioral characterization of the new potent nonselective dopamine agonist pergolide.

Pergolide (LY127809, CAS 66104-23-2), a non-selective dopamine agonist, was evaluated for broad behavioral properties in a wide range of pharmacological tests. The selective dopamine2(D2) agonist, bromocriptine, served as a reference standard for those tests where behavioral activity was noted with pergolide. Pergolide and bromocriptine were administered orally to mice at doses of 0.3-30 and 3-300 mg/kg, respectively. Both compounds produced biphasic effects on spontaneous activity, increased hexobarbital-induced sleep time, and lowered mouse body temperature. Qualitative changes with pergolide were observed with some mice showing hyporeactiveness, ptosis, slowed respiration and placing loss. Reserpine-induced hypothermia was reversed by pergolide with significant increases in the body temperature of reserpine-treated mice. However, a further reduction in the body temperature of reserpinized hypothermic mice was seen following bromocriptine administration. Acetic acid-induced writhing and performance on the rotarod were both impaired by higher doses of pergolide. Bromocriptine administration also reduced writhing at higher doses but did not alter performance on the rotarod. Pergolide had no effect on seizure activity as evaluated by electroshock, pentylenetetrazol (pentetrazol) or strychnine. Oxotremorine-induced tremors and salivation, grip strength, and tail-flick were not affected by pergolide. Neither pergolide nor bromocriptine altered established shuttle-avoidance behavior in rats at oral doses of 0.1 to 30 mg/kg. Behavioral assessment of pergolide in dogs was complicated by severe emetic responses at clinically relevant doses greater than 0.003 mg/kg. In summary, these data suggest that pergolide produces a behavioral profile which is characteristic of dopaminergics.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗
PubMed1991

Anti-inflammatory activity of pergolide, a dopamine receptor agonist.

Pergolide, a dopamine agonist effective in the treatment of Parkinson's disease, has been shown to have anti-inflammatory activity in the carrageenan paw edema assay in rats at p.o. doses greater than or equal to 0.3 mg/kg. Studies were done to investigate the mechanism of action and to determine the pharmacologic significance of this finding. Because pergolide elevates circulating glucocorticoids, the effect of pergolide on carrageenan-induced paw swelling was assessed in adrenalectomized rats. Pergolide retained its anti-inflammatory activity in adrenalectomized carrageenan-injected rats, thus eliminating corticosterone induction as a possible mechanism of action. Pergolide treatment also did not decrease thromboxane B2, prostaglandin E2 or leukotriene B4 production, ruling out direct effects on arachnoid acid inflammatory mediators. Interactions with the autonomic nervous system were suggested, in that an alpha adrenergic agonist (clonidine) mimicked the activity of pergolide in the carrageenan assay, and an alpha adrenergic antagonist (phenoxybenzamine) blocked the anti-inflammatory activity of pergolide in this assay. Dopamine receptor antagonists (haloperidol or sulpiride) partially inhibited the effect of pergolide in the carrageenan model. However, the peripherally restricted dopamine antagonist, domperidone, was ineffective, suggesting that a central dopamine receptor was involved in the effect. Experiments in chronic inflammation models such as lipoidal-amine induced arthritis in rats and picryl chloride-induced delayed type hypersensitivity in mice also revealed an anti-inflammatory effect of pergolide. Activity in the carrageenan system and the lipoidalamine model demonstrated that the anti-inflammatory effects of pergolide were separable from potential immunosuppressive effects. Multiple dose studies indicated that tolerance might develop to the anti-inflammatory effect of pergolide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Characterization of the neurogenic vasodilatation elicited by central dopamine receptor stimulation with pergolide.

In the present study, we have employed the procedure of bilateral hindlimb perfusion at controlled flow rates to investigate centrally mediated actions of the dopamine receptor agonist pergolide on hindlimb vascular resistance in anesthetized dogs. Intracisternal administration of pergolide caused sustained hypotension, bradycardia and a decrease in perfusion pressure in the innervated hindlimb, whereas perfusion pressure in the denervated limb was not altered by pergolide. In addition, the pressure-flow curves were shifted to the right in the innervated hindlimb but not in the denervated limb, suggesting that pergolide caused neurogenic dilatation in the hindlimb vasculature. Intravenous administration of the same dose of pergolide elicited transient hypertension and marked vasoconstriction in the denervated limb. Hypotension and neurogenic hindlimb vasodilatation of lesser magnitude than that produced by intracisternal pergolide were seen only 40 to 50 min after administration of i.v. pergolide. The hindlimb vasodilator action of intracisternal pergolide could be antagonized by sulpiride, which suggests that activation of central dopamine receptors was responsible for the action of pergolide. Because the neural innervation to the hindlimb is comprised of sympathetic vasoconstrictor as well as cholinergic and dopaminergic vasodilator fibers, additional experiments were performed to determine the mechanisms involved in the neurogenic vasodilatation caused by pergolide. Treatment with atropine did not alter the neurogenic decrease in the hindlimb vascular resistance produced by pergolide, indicating that activation of cholinergic vasodilator fibers was not responsible for this phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Differential effects of quinelorane and pergolide on behaviour, blood pressure, and body temperature of spontaneously hypertensive rats and Wistar-Kyoto rats.

The systemic administration of the dopamine agonists quinelorane or pergolide to Wistar-Kyoto rats (WKY) induced a significant increase of locomotor activity at higher doses. In spontaneously hypertensive rats, these compounds induced a significant hypoactivity at low doses, but only a modest, and late, increase in locomotor activity at higher doses. Quinelorane was more potent than pergolide on locomotor activity. In WKY and SHR, which had unilateral lesions of the nigrostriatal dopamine system, quinelorane and pergolide induced similar dose-dependent contralateral turning that, in the case of pergolide, was significantly greater in SHR than in WKY. Both quinelorane and pergolide induced yawning similarly in WKY and SHR, and quinelorane was more potent than pergolide. The intravenous administration of quinelorane induced an immediate and dose-dependent increase in blood pressure in WKY and SHR, which could be completely prevented by pretreating the rats with the dopamine antagonist haloperidol. Pergolide similarly caused a rise in blood pressure in WKY and SHR, but its effect could only partially be blocked by haloperidol. The subcutaneous injection of quinelorane or pergolide induced similar dose-dependent hypothermia in WKY. Pergolide also caused a decrease of body temperature in SHR, but quinelorane had little effect in this strain. These results show differences in the effects of quinelorane and pergolide between various experimental test situations and between WKY and SHR. These differences may be related to the involvement of dopamine receptor subtypes and to the previously described changes in central dopaminergic activity in SHR.

Animals↗
PubMed1995

A crossover, controlled study comparing pergolide with bromocriptine as an adjunct to levodopa for the treatment of Parkinson's disease.

A single-blind, crossover study was carried out to compare the efficacy and safety of pergolide against that of bromocriptine in 57 patients with Parkinson's disease who showed a declining response to levodopa therapy. Patients were randomly assigned to receive either bromocriptine followed by pergolide, or pergolide followed by bromocriptine. Both drugs were administered for 12 weeks. Patients were assessed by a clinician blinded to treatment assignment using the New York University Parkinson's Disease Scale. The average daily dose of pergolide was 2.3 +/- 0.8 mg and of bromocriptine 24.2 +/- 8.4 mg. Addition of pergolide or bromocriptine resulted in a significant improvement in total scores when compared with the previous treatment of levodopa alone (pergolide, p = 0.0001; bromocriptine, p = 0.0005). Pergolide was more effective than bromocriptine in daily living scores (p = 0.02) and motor scores (p = 0.038). No differences in the incidence of dyskinesias, dystonias, or psychosis were observed between groups. Fewer adverse events were recorded in the pergolide group, and 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↗