Dopaminergic stimulation of prolactin release.
Prolactin (PRL) secretion from anterior pituitary is believed to be under tonic inhibitory control of dopamine (DA) released from the tubero-infundibular dopaminergic neurones into the hypophysial portal blood. Inhibition of PRL release by DA seems to be mediated by sereospecific DA receptors located in PRL cells. Apomorphine and various ergot alkaloids such as bromocryptine mimic the inhibitory effect of DA both in vivo and in vitro, presumably by a direct agonist action on these 'inhibitory' receptors. We now report that PRL secretion in primary cultures of rat pituitary cells can be stimulated by DA when concentrations a thousand times lower than those required for inhibition are used. Secretion rates above basal release can also be induced by apomorphine and bromocryptine when the 'inhibitory' receptors are blocked with certain DA receptor antagonists.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001971:Bromocriptine / Q000494:pharmacology; D002069:Butaclamol / Q000494:pharmacology; D002478:Cells, Cultured; D004298:Dopamine / Q000494:pharmacology*; D006220:Haloperidol / Q000494:pharmacology; D008297:Male; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism*; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects
D011954:Receptors, Dopamine; D001971:Bromocriptine; D011388:Prolactin; D002069:Butaclamol; D006220:Haloperidol; D001058:Apomorphine; D004298:Dopamine