The Cardiovascular Effects of Bromocriptine in Parkinsonism

Greenacre, J.K.; Teychenne, Paul F.; Petrie, Aviva; Calne, D. B.; Leigh, P. Nigel; Reid, John L.

doi:10.1111/j.1365-2125.1976.tb04877.x

Cited by 40 publications

(8 citation statements)

References 14 publications

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“…In these respects, it contrasts with the smooth, dose-dependent lowering of blood pressure discussed above. Although collapse of blood pressure has been described occurring after the first, 2 5 mg, dose of bromocriptine, 7 perhaps on an idiosyncratic basis, none of our patients experienced this. In patients with idiopathic Parkinson's disease, therefore, the appearance of significant postural hypotension is not necessarily an indication for either abandoning bromocriptine, lowering the dose, or altering the rate of dose increase.…”

Section: Discussionmentioning

confidence: 54%

Bromocriptine in Parkinson's disease: a study of cardiovascular effects.

Quinn¹,

Illas²,

Lhermitte³

et al. 1981

Journal of Neurology, Neurosurgery & Psychiatry

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SUMMARY Blood pressure and pulse rate were studied in 20 Parkinsonian patients on no treatment, and during treatment with bromocriptine (mean dosage 148 mg/day) as the sole anti-Parkinsonian therapy. The drug was shown to reduce erect systolic and diastolic and supine systolic blood pressure and to increase erect pulse rate, in a predictable dose-dependent manner. The occurrence of episodes of significant postural hypotension was less predictable and was a transitory phenomenon in all patients. Peripheral dopamine receptor blockade with domperidone did not alter the findings, suggesting that the principal mechanism for these cardiovascular effects is a central dopaminergic one.In Parkinson's disease oral levodopa lowers systolic and diastolic blood pressure both in the lying and, to a greater degree, in the standing position.'-3 When levodopa is administered together with a peripheral DOPA-decarboxylase inhibitor, the same effects are observed,4-6 suggesting that levodopa-induced hypotension is principally centrally mediated.Bromocriptine lowers blood pressure in patients with Parkinson's disease,7 8 acromegaly9 and essential hypertension.'01" In the studies cited it was administered either in low dosage, often together with levodopa7 or a-methyl DOPA,"1 or as single variable doses. Patients and methodsTwenty patients with Parkinson's disease were studied. Subjects with a history of symptomatic orthostatic hypotension were excluded. All 17 patients previously on levodopa stopped this medication on admission; all but one stopped all other anti-Parkinsonian medication. One patient already taking a 3-blocker for angina continued with the same dosage. The initial assessment of Parkinsonian and cardiovascular status took place 24-72 hours after stopping treatment, and the last set of results off treatment was taken as the control series. Bromocriptine was then introduced, starting with one 2 5 mg tablet and adding one tablet successively to the three daily doses, giving a constant increase of total dose of 22 5 mg/day. This rapid rate of increase was permitted by the introduction of domperidone 50 mg thrice daily, as an antiemetic. When high clinically optimal (mean improvement over baseline of 75%)13 doses of bromocriptine (mean 148 mg/day) were reached, all 20 patients were taking active domperidone (phase A). Placebo domperidone was then introduced (phase B) in all patients for a period of I to 5 (mean 2 2) days.The patients were studied for 10 to 15 (mean 12) days. Systolic and diastolic pressures (measured manually) and pulse were recorded daily, after 5 minutes supine, immediately on standing, and after 1 minute and 5 minutes erect. Two hundred and thirty-four blood pressure readings were taken. Statistical analysis was performed using the t pair test. 426by copyright.

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Section: Discussionmentioning

confidence: 54%

Bromocriptine in Parkinson's disease: a study of cardiovascular effects.

Quinn¹,

Illas²,

Lhermitte³

et al. 1981

Journal of Neurology, Neurosurgery & Psychiatry

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“…L-dopa and dopamine agonists reduce supine systolic BP and induce orthostatic hypotension with reflex tachycardia. [14][15][16][17][18] Because selegiline in combination with L-dopa caused orthostatic hypotension without tachycardia and possibly also exerted a supine pressor effect, it appears that the mechanism(s) underlying the cardiovascular effects of this therapeutic regimen are distinct from those attributable to L-dopa alone. Loss of selectivity for MAOB with long-term selegiline therapy 19,20 causing increased levels of circulating tyramine, 21 or metabolism of selegiline to met-amphetamine and amphetamine, [22][23][24][25][26] could cause orthostatic hypotension.…”

Section: Discussionmentioning

confidence: 95%

Selegiline-induced postural hypotension in Parkinson's disease: A longitudinal study on the effects of drug withdrawal

1999

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“…Postural hypotension is one side effect of the clinical use of the dopamine agonist, bromocriptine, in the treatment of parkinsonism, acromegaly and infertility (O'Mullane, Davis, Hipkin & Walker, 1976; Greenacre, Teychenn, Petrie, Calne, Leigh & Reid, 1976;Brosens, 1977;Linch, Shaw, Muhlemann & Ross, 1978;Price, Debono, Parkes, Marsden & Rosenthaler, 1978). In the treatment of hypertension, bromocriptine has been used successfully either alone (Stumpe, Kollock, Higuchi, Kruck & Vetter, 1977) or in combination with other antihypertensive drugs (Kaye, Shaw & Ross, 1976;Lewis, Henderson & Fisher, 1976).…”

Section: Introductionmentioning

confidence: 99%

Involvement of the Adrenal Glands in the Hypotensive Response to Bromocriptine in Spontaneously Hypertensive Rats

Hamilton

1981

British J Pharmacology

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1 The dopamine agonist, bromocriptine, produced a hypotensive response following oral administration to conscious normotensive and spontaneously hypertensive (SH-) rats. 2 In SH-rats the dose-related falls in blood pressure to bromocriptine, 3 to 30 mg/kg orally or intraperitoneally, were biphasic, an initial fall at 1 h being followed by some recovery at 2 h and a subsequent fall in blood pressure at 4 and 6 h.3 The dopamine antagonists, metoclopramide, sulpiride, haloperidol and pimozide, had little or no effect on the hypotensive response to bromocriptine, 10 mg/kg orally, in SH-rats. 4 Pretreatment with a-methyl-p-tyrosine augmented the hypotensive response to bromocriptine, 10 mg/kg orally, in SH-rats.5 In adrenal demedullated SH-rats, the hypotensive response to bromocriptine, 3 to 30 mg/kg orally, was abolished.6 In SH-rats the hypotensive response to bromocriptine, 10 mg/kg orally, was prevented by the ,3-adrenoceptor blocking drugs, propranolol and oxprenolol, but was unaffected by (+)-propranolol and by the cardio-selective ,8-adrenoceptor blocking drug, atenolol. 7 In SH-rats pretreated with bromocriptine, 10 mg/kg orally, and then anaesthetized, the pressor responses to low doses of intravenous adrenaline were reversed to depressor, indicating that bromocriptine possesses a-adrenoceptor blocking activity.8 The results suggest that the hypotensive response to bromocriptine in conscious SH-rats is mediated by adrenaline released from the adrenal medullae which, in the presence of a-adrenoceptor blockade, stimulates vascular,f-adrenoceptors producing vasodilatation.

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The Cardiovascular Effects of Bromocriptine in Parkinsonism

Cited by 40 publications

References 14 publications

Bromocriptine in Parkinson's disease: a study of cardiovascular effects.

Bromocriptine in Parkinson's disease: a study of cardiovascular effects.

Selegiline-induced postural hypotension in Parkinson's disease: A longitudinal study on the effects of drug withdrawal

Involvement of the Adrenal Glands in the Hypotensive Response to Bromocriptine in Spontaneously Hypertensive Rats

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