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Pharmacology · Drugs and Prescriptions

Bromocriptine

Bromokriptinum

Bromocriptine is a semisynthetic ergot alkaloid derivative (ergocryptine) belonging to the group of central nervous system agents. It is a direct dopamine receptor agonist, which provides pronounced antiparkinsonian and endocrine effects.

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Dosage formsTablets (0.0025 g), capsules (0.005 and 0.01 g)
TargetD1 and D2 dopamine receptors (predominantly D2)
Endocrine effectDecreases the secretion of prolactin and growth hormone (somatotropic hormone, STH)
PharmacokineticsExceeds levodopa in duration of action
How to write a prescription
Rp.: Tab. Bromokriptini 0,0025
D.t.d. N 30
S. Внутрь по 1/2 таблетки 1 раз в сутки вечером во время еды

Alternative spellings: Tab. Bromocriptini 0,0025; Tabulettas Bromokriptini 0,0025; Caps. Bromocriptini 0,005

Dosage form
Tablets 0.0025 g each; capsules 0.005 and 0.01 g each
Administration
Orally 0.00125 g (1/2 tab.), to be taken in the evening
Group
Agents affecting the central nervous system
3 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Classification position

In the pharmacotherapy of Parkinson's disease, bromocriptine belongs to agents that stimulate the dopaminergic system, specifically to direct dopamine receptor stimulants (agonists).

For differential diagnosis, it is important to distinguish it from other groups:

  • Levodopa is a dopamine precursor.
  • Selegiline is an MAO-B inhibitor.
  • Amantadine is an agent that increases dopamine release (and an NMDA receptor blocker).
  • Trihexyphenidyl is a central anticholinergic agent (suppresses the cholinergic system).

Mechanism of action

The drug is a non-selective agonist of $D_1$ and $D_2$ receptors, but exhibits the highest specific activity precisely toward $D_2$ receptors.

Unlike levodopa, which requires metabolic conversion to dopamine to cross the blood-brain barrier, bromocriptine provides direct excitation of postsynaptic dopamine receptors in the CNS.

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Pharmacological effects

The drug's effect strictly depends on the localization of the stimulated receptors:

  1. Antiparkinsonian effect: mediated by stimulation of $D_2$ receptors in the neostriatum.
  2. Endocrine effect: stimulation of pituitary $D_2$ receptors leads to decreased hormone release from the anterior lobe.
  3. Effect on the prolactin axis: normally, the hypothalamus exerts dual control over lactation, with dopamine acting as the primary inhibitory factor. Bromocriptine mimics this effect, suppressing the secretion of lactotropic hormone (prolactin).
  4. Effect on the somatotropic axis: the drug is also capable of reducing growth hormone (STH) secretion.

Indications for use

The drug is used in both neurology and endocrinology:

  • Parkinson's disease: prescribed predominantly in combination with levodopa. The combination is justified when levodopa is insufficiently effective or when the "on-off" phenomenon develops.
  • Hyperprolactinemic states: prolactin-dependent amenorrhea, galactorrhea.
  • Lactation: used for the pharmacological cessation of physiological lactation.
  • Acromegaly: prescribed to suppress STH when surgical treatment is not feasible.

Comparison with other dopamine agonists

Other drugs of this group are also used in modern practice:

  • Pramipexole: stimulates $D_2$ and $D_3$ receptors. It is considered more effective than bromocriptine and can be used either as monotherapy or with levodopa.
  • Cabergoline (Dostinex): a modern selective $D_2$ receptor agonist. It features a significantly longer duration of action (the hypoprolactinemic effect persists for 7–28 days). At therapeutic doses, it suppresses only pituitary lactotrophs, and only at high doses does it cause central stimulation effects.

Side effects and contraindications

The side effects of bromocriptine have a clear pathogenetic connection with the localization of dopamine receptors in the body:

  • Chemoreceptor trigger zone of the vomiting center: nausea and vomiting.
  • Cerebral cortex: psychotic reactions (delusions, hallucinations).
  • Extrapyramidal system: dyskinesias.
  • Peripheral circulation: orthostatic reactions, as well as peripheral arterial spasm, which can lead to calf muscle cramps.
  • Other: dry mouth, constipation.

Contraindications: severe forms of arterial hypertension, occlusive vascular diseases, Huntington's chorea.

Briefly: answers to topical questions

What are the pharmacokinetic parameters of bromocriptine (bioavailability, metabolism, half-life)?

Exact pharmacokinetic parameters of bromocriptine, such as bioavailability, metabolic pathways, and half-life, are not described in the sources.

The study materials present only one comparative characteristic of the drug:

  • Bromocriptine (Bromocriptine) — has a pharmacokinetic advantage, as it exceeds levodopa in duration of action.

Other quantitative or qualitative indicators of this drug's pharmacokinetics are completely absent from the provided texts.

How to memorize

BROMocriptine BRINGS prolactin levels down and directly inhibits Parkinson's (direct D2 agonist).

Class and exam questions

What is the principal difference in the mechanism of action between bromocriptine and levodopa?

Levodopa is merely a precursor that requires metabolic conversion to dopamine. Bromocriptine is a direct agonist; it directly excites dopamine receptors in the neostriatum itself.

Why does bromocriptine cause nausea and vomiting?

The drug stimulates dopamine receptors in the trigger zone of the vomiting center, which leads to activation of the vomiting reflex.

Why is bromocriptine prescribed for acromegaly?

Stimulation of pituitary D2 receptors by bromocriptine leads to a decrease in the secretion of not only prolactin, but also growth hormone (STH), an excess of which causes acromegaly.

Why is cabergoline better than bromocriptine for suppressing lactation?

Cabergoline is a highly selective D2 receptor agonist and acts significantly longer (up to 28 days), making it a more convenient and modern drug.

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What else to study on this topic

  • Classification of antiparkinsonian drugs by their effect on neurotransmitter systems
  • Pharmacokinetics of levodopa and the rationale for its combination with carbidopa
  • Physiology of the prolactin axis: dual hypothalamic control
  • Somatotropic axis: somatostatin, GHRH, and their synthetic analogues (octreotide, sermorelin)
  • Comparative characteristics of dopamine receptor agonists (bromocriptine, pramipexole, cabergoline)

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