Bromocriptine

Reference

A dopamine receptor agonist with selective agonist activity on D2 dopamine receptors while simultaneously acting as a partial antagonist for D1 dopamine receptors

Bromocriptine binds directly to striatal dopamine D2 receptors → replacing the degeneration of dopaminergic nigrostriatal neurons → stimulating locomotion and attenuating the bradykinetic symptoms.

Bromocriptine binds directly to dopamine D2 receptors of anterior pituitary lactotrophic cells → blocks prolactin exocytosis and gene expression

Bromocriptine binds directly to D2-dopamine receptor on anterior pituitary somatotrophic tumour cells → dopaminergic effect can cause paradoxical blocking of GH release through tuberoinfundibular pathways, decreasing circulating blood concentrations of GH
Hjortebjerg 2017 Physiologically, dopamine stimulates GH secretion, but dopamine receptor agonists paradoxically suppress GH hypersecretion in acromegalic patients through binding to D2 receptors on adenomas

Bromocriptine resets dopaminergic and sympathetic tone within the CNS → sympatholytic effect that decreases metabolic processes, which can lead to glucose tolerance and insulin sensitivity.

These states depends on monoamine neurotransmitter (dopamine (DA), serotonin (5-HT), noradrenaline (NA) and histamine) concentrations in the

Initial dose of 1.25 to 2.50 mg/day
Increase in 2.50 mg increments until desired GH blood concentrations are reached

Initial dose of 2.50 mg/day
Increase in increments of 2.50 mg based on tolerance and effect.
Use the lowest dose possible to achieve symptomatic control, with a low dose considered less than 30.0 mg/day and a high dose considered 31.0 to 100 mg/day.

Initial dose of 0.8 mg/day with a weekly increase of 0.8 mg until the desired glycemic control is reached, with a maximum dose of 4.80 mg/day.