Every once in a while, a drug appears that changes the practice of medicine, alters methods of treatment, and forces practitioners to rethink and reformulate their concepts of pathophysiology. Penicillin, cortisone, and propranolol hydrochloride are drugs that would fit that description; doubtless there are others as well that one could, if one were so inclined, also name. My current candidate for this distinction is bromocriptine.1
A semisynthetic alkaloid of the ergot family, bromocriptine (2-Br-a-ergokryptine mesylate) was formulated in 1967. Several years later the drug was shown to stimulate dopamine receptors and to compete with the binding of naturally occurring dopamine at its neurological receptor sites.2-4 Since prolactin secretion is under the inhibitory control of dopamine, a hypothalamic catecholamine, it was soon demonstrated that bromocriptine would inhibit prolactin secretion; furthermore, that inhibition is remarkably successful. For example, after a single therapeutic dose of bromocriptine, serum prolactin levels remain suppressed
Dalessio DJ. Internal Medicine. JAMA. 1984;252(16):2167–2172. doi:10.1001/jama.1984.03350160035013
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