Matsushita N, Kato Y, Katakami H, Shimatsu A, Yanaihara N, Imura H
Proc Soc Exp Biol Med. 1983 Jan;172(1):118-21. doi: 10.3181/00379727-172-1-rc1.
Synthetic gastrin releasing peptide (GRP) injected intraventricularly (1 microgram/rat), but not intravenously, suppressed rat prolactin (PRL) release induced by a Met-enkephalin analog, FK33-824 (10 micrograms/100 g body wt., iv). GRP also blunted PRL release induced by a dopamine antagonist, domperidone (1 microgram/100 g body wt., iv). In contrast, GRP did not suppress elevated plasma PRL levels sustained by a large dose of domperidone (10 micrograms/100 g body wt., iv). GRP (10(-5) M) had no effect on PRL release from superfused pituitary cells in vitro. These results suggest that GRP inhibits PRL secretion in the rat by acting through the brain to stimulate the dopaminergic mechanism.
脑室内注射(每只大鼠1微克)而非静脉注射的合成胃泌素释放肽(GRP),可抑制由甲硫氨酸脑啡肽类似物FK33 - 824(10微克/100克体重,静脉注射)诱导的大鼠催乳素(PRL)释放。GRP还能减弱由多巴胺拮抗剂多潘立酮(1微克/100克体重,静脉注射)诱导的PRL释放。相比之下,GRP并不能抑制大剂量多潘立酮(10微克/100克体重,静脉注射)维持的血浆PRL水平升高。GRP(10⁻⁵ M)对体外灌流垂体细胞的PRL释放没有影响。这些结果表明,GRP通过作用于大脑刺激多巴胺能机制来抑制大鼠的PRL分泌。