Mai L M, Pan J T
Institute of Physiology, National Yang-Ming Medical College, Taipei, Taiwan, Republic of China.
Life Sci. 1990;47(14):1243-51. doi: 10.1016/0024-3205(90)90217-f.
The roles of oxytocin (OT) and vasopressin (AVP) on both basal and estrogen-induced prolactin (PRL) secretion were examined. Adult female Sprague-Dawley rats that were ovariectomized for 3 weeks and received estrogen treatment for 1 week were used. Intravenous administration of hormones and serial blood sampling were accomplished through indwelling intraatrial catheters which were implanted two days before. Plasma PRL levels were measured by radioimmunoassay. Oxytocin at a dose of 20 micrograms/rat stimulated a moderate PRL release in the morning and lower doses (5 and 10 micrograms) were without effect. Vasopressin was most effective at a dose of 5 micrograms/rat in stimulating PRL release, while consecutive injections of higher doses (10 and 20 micrograms) were less effective. In contrast, TRH, ranging from 1 to 8 micrograms/rat, induced a dose-dependent increases in PRL secretion. Using the effective dosages determined from the morning studies, repeated injections of either OT, AVP or their specific antagonists MPOMeOVT [( 1-(beta-mercapto-beta, beta-cyclopentamethylene propanoic acid), 2-(O-methyl)tyrosine, 8-ornithine]-vasotocin) and d (CH2)5Tyr(Me)AVP ([1-(beta-mercapto-beta, beta-cyclo-pentamethylene propionic acid), 2-(O-methyl)tyrosine, 8-arginine]-vasopressin), were given hourly between 1300 to 1800 h and blood samples were obtained hourly from 1100 to 1900 h. It was found that either OT or AVP significantly reduced the afternoon PRL surge, while their antagonists were not as effective. When OT or AVP were administered together with their specific antagonists, the inhibitory effects of either hormone on PRL surge were reversed. Thus it is concluded that both OT and AVP assume a non-specific stress-like effect on PRL release, in which basal secretion is stimulated and surge secretion is inhibited.
研究了催产素(OT)和血管加压素(AVP)对基础催乳素(PRL)分泌以及雌激素诱导的PRL分泌的作用。使用成年雌性Sprague-Dawley大鼠,这些大鼠已卵巢切除3周并接受雌激素治疗1周。通过两天前植入的留置心房导管进行激素的静脉内给药和系列采血。通过放射免疫测定法测量血浆PRL水平。剂量为20微克/大鼠的催产素在早晨刺激了适度的PRL释放,而较低剂量(5和10微克)则无作用。血管加压素在剂量为5微克/大鼠时对刺激PRL释放最有效,而连续注射较高剂量(10和20微克)则效果较差。相比之下,剂量为1至8微克/大鼠的促甲状腺激素释放激素(TRH)诱导PRL分泌呈剂量依赖性增加。使用早晨研究确定的有效剂量,在1300至1800 h之间每小时重复注射OT、AVP或它们的特异性拮抗剂MPOMeOVT [(1-(β-巯基-β,β-环戊亚甲基丙酸),2-(O-甲基)酪氨酸,8-鸟氨酸]-加压素)和d(CH2)5Tyr(Me)AVP [(1-(β-巯基-β,β-环戊亚甲基丙酸),2-(O-甲基)酪氨酸,8-精氨酸]-血管加压素),并在1100至1900 h每小时采集血样。发现OT或AVP均显著降低下午的PRL峰值,而它们的拮抗剂效果不佳。当OT或AVP与它们的特异性拮抗剂一起给药时,两种激素对PRL峰值的抑制作用均被逆转。因此得出结论,OT和AVP对PRL释放均具有非特异性的应激样作用,其中基础分泌受到刺激而峰值分泌受到抑制。