Myers L S, Steele M K
Department of Psychology, CSU, Stanislaus, Turlock, California 95380.
Endocrinology. 1991 Oct;129(4):1744-8. doi: 10.1210/endo-129-4-1744.
The present studies investigated the role of the brain renin-angiotensin system in the regulation of PRL secretion in the male rat. Blood samples were taken from conscious rats before, during, and after administration of test substances into the third cerebral ventricle. In the first series of experiments, we determined the sensitivity of the PRL response to intracerebroventricular (icv) administration of angiotensin II (Ang II) and found that PRL levels were significantly suppressed in a dose-related manner (10-500 ng). A dose of 1 ng did not significantly affect PRL values, compared to those from vehicle-injected animals. Ang II elicited water intake at doses of 50 and 500 ng, but not at the 10- or 1-ng doses. In the second series of experiments, we investigated the role of endogenous brain Ang II in the regulation of PRL secretion under basal and stimulated conditions. The endogenous system was manipulated by icv infusion of saralasin, an Ang II receptor antagonist, or icv injection of enalaprilat, a converting enzyme inhibitor, to prevent synthesis of Ang II. Neither saralasin nor enalaprilat administration produced an increase in PRL levels under basal, nonstressed conditions. However, during immobilization stress, when PRL levels increased 3-fold during icv vehicle infusion, saralasin infusion resulted in a 7-fold rise in plasma PRL titers relative to prestress baseline values. These results demonstrate that, in male rats, the inhibitory effects of icv administration of Ang II on PRL secretion are very sensitive and are observed at doses which do not affect water intake. The endogenous brain Ang II system appears not to be involved in the maintenance of the low plasma PRL levels observed under basal, nonstressed conditions. However, the system does appear to affect the magnitude of the PRL response to immobilization stress.
本研究调查了脑肾素-血管紧张素系统在雄性大鼠催乳素（PRL）分泌调节中的作用。在向第三脑室注射测试物质之前、期间和之后，从清醒大鼠采集血样。在第一系列实验中，我们测定了PRL对脑室内（icv）注射血管紧张素II（Ang II）反应的敏感性，发现PRL水平以剂量相关方式（10 - 500 ng）显著受到抑制。与注射赋形剂的动物相比，1 ng剂量对PRL值无显著影响。50和500 ng剂量的Ang II引起水摄入，但10 ng或1 ng剂量则不会。在第二系列实验中，我们研究了内源性脑Ang II在基础和刺激条件下对PRL分泌调节中的作用。通过icv输注Ang II受体拮抗剂沙拉新或icv注射转化酶抑制剂依那普利拉来操纵内源性系统，以阻止Ang II的合成。在基础、无应激条件下，给予沙拉新或依那普利拉均未使PRL水平升高。然而，在固定应激期间，当icv注射赋形剂时PRL水平增加3倍，输注沙拉新导致血浆PRL滴度相对于应激前基线值升高7倍。这些结果表明，在雄性大鼠中，icv注射Ang II对PRL分泌的抑制作用非常敏感，且在不影响水摄入的剂量下即可观察到。内源性脑Ang II系统似乎不参与基础、无应激条件下观察到的低血浆PRL水平的维持。然而，该系统似乎确实影响PRL对固定应激反应的幅度。
