The regulatory mechanism of endothelin on the secretion of the pituitary horones

1. (1)用免疫组织化学方法研究了牛蛙脑垂体内皮素3（ET 3）样免疫反应阳性物质的分布。ET-3免疫反应（ET-3-IR）细胞被发现对应于显示LH-和FSH -免疫反应的细胞。在雄性垂体中，仅观察到少数ET 3-ir细胞。(2)胶体金免疫电镜分析显示ET 3样物质和促性腺激素在同一分泌颗粒内共存。提示ET 3可能作为一种自分泌和/或旁分泌因子参与垂体功能调节.用大鼠ET B受体（ET_B受体）第425-439位氨基酸制备抗血清。在正中隆起和终板血管器内可见大量ET_B受体阳性纤维。用抗黄体生成素释放激素（LHRH）抗血清双标法研究表明，在这些区域内，ET_B受体样免疫反应与LHRH免疫反应纤维相关。在LHRH阳性胞体中未检测到ET_B受体样免疫反应。这一结果表明ET通过终末野轴突上的ET_B受体影响LHRH神经系统。本文观察了内皮素（ET-1）对大鼠离体神经叶加压素（VP）释放的影响。此外，还研究了血管紧张素II（ANG II）的作用，因为它与ET-1和VP共定位于轴突终末的相同分泌颗粒中。ET-1诱导VP释放增加，随后在其撤药后下降至基础水平。这些结果表明ET-1和ANG Ⅱ直接作用于神经叶，刺激VP的释放，但其作用部位尚不清楚。

1. (1) The distribution of endothelin-3 (ET3)-like immunoreactivity in the bullfrog pituitary was investigated immunohistochemically. ET3-immunoreactive (ET3-ir) cells were found to correspond to cells showing LH- and FSH -immunoreactivities. In the male pituitary, only a few ET3-ir cells were observed. (2) Immuno-electron microscopic analysis using colloidal gold revealed the co-existence of ET3-like substance (s) and gonadotropins within the same secretory granules. These results suggest the possible participation of ET3 in regulating pituitary function as an autocrine and/or paractrine hormone.2. Antisera were raised against amino-acid residues 425-439 of the rat ET B receptor (ET_B receptor). Massive ET_B receptor immunoreactive fibers were observed in the median eminence and organum vasculosum lamina terminalis of rats. Double labeling studies with antiluteinzing hormone-releasing hormone (LHRH) antiserum revealed that ET_B receptor-like immunoreactivity associated with LHRH-immunoreactive fibers in these areas. However, ET_B receptor-like immunoreactivity was not detected in LHRH-immunoreactive somata. This result suggests that ET affects the LHRH neuronal systems via ET_B receptors on the axon at the terminal field.3. Effects of ET-1 on the release of vasopressin (VP) from the isolated neural lobe of the rat were investigated. In addition, effects of angiotensin II (ANG II) were also investigated, because it colocalizes with ET-1 and VP in the same secretory granules in the axon terminals. ET-1 induced an increase in VP release, followed by a decline to basal levels upon its withdrawal. The VP release was also stimulated by ANG II.These results strongly suggest that ET-1 and ANG II act directly on the neural lobe to stimulate the release of VP.However, the sites of action of these peptides are not clear.