STIMULATION OF HYPOTHALAMIC PROLACTIN-RELEASE BY VERATRIDINE AND ANGIOTENSIN-II IN THE FEMALE RAT - EFFECT OF OVARIECTOMY AND ESTRADIOL ADMINISTRATION
STIMULATION OF HYPOTHALAMIC PROLACTIN-RELEASE BY VERATRIDINE AND ANGIOTENSIN-II IN THE FEMALE RAT - EFFECT OF OVARIECTOMY AND ESTRADIOL ADMINISTRATION
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DOI：
10.1159/000125919
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发表时间：
1991-10-01
影响因子：
4.1
通讯作者：
AVAKIAN, C
中科院分区：
文献类型：
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作者：
DEVITO, WJ;STONE, S;AVAKIAN, C
在雌性大鼠的下丘脑和其他脑区中发现了免疫反应性催乳素（IR-PRL）。 脑IR-PRL不是垂体起源的，并且基于聚丙烯酰胺凝胶电泳和肽图谱，与其垂体对应物具有高度的序列同源性。 我们以前已经表明，下丘脑组织可以释放IR-PRL在体外时，钾去极化。 在这项研究中，我们研究了释放IR-PRL从下丘脑获得的完整和卵巢切除大鼠和孵育的存在下，藜芦碱（生物碱去极化兴奋膜），血管紧张素II，或促甲状腺激素释放激素。 下丘脑组织自发地释放IR-PRL，并且这种释放以剂量依赖性方式被藜芦碱或血管紧张素II显著增加。 血管紧张素II受体拮抗剂saralasin对下丘脑IR-PRL释放的抑制作用证明了血管紧张素II诱导IR-PRL释放的特异性。 促甲状腺激素释放激素（100 μ M）对下丘脑IR-PRL的释放没有影响。 卵巢切除术降低下丘脑IR-PRL含量和IR-PRL释放的反应，阿曲库铵和血管紧张素II。 还通过从注射雌二醇（1 μ g/天）或赋形剂5天的卵巢切除大鼠获得下丘脑来检查雌二醇对下丘脑IR-PRL含量和释放的影响。 与注射溶剂的大鼠相比，给予雌二醇显著增加了下丘脑IR-PRL含量（46 +/- 4 vs. 81 +/- 16 ng/mg蛋白）。 在相同的大鼠中，与注射溶剂的大鼠相比，藜芦碱（100 mM; 7.26 +/- 0.97 vs. 10.4 +/- 1.46 ng/ml）和血管紧张素II（1 μ M; 5.08 +/- 0.84 vs. 9.9 +/- 1.2 ng/ml）刺激的IR-PRL释放显着增加。 这些数据表明，血管紧张素II，而不是促甲状腺激素释放激素，刺激释放的IR-PRL从女性下丘脑。 下丘脑IR-PRL含量和雌二醇释放的增加表明，雌二醇刺激下丘脑IR-PRL合成，导致IR-PRL可释放池的增加。
In the female rat immunoreactive prolactin (IR-PRL) has been identified in the hypothalamus and in other brain regions. Brain IR-PRL is not of pituitary origin and, based on polyacrylamide gel electrophoresis and peptide mapping, shares a high degree of sequence homology with its pituitary counterpart. We have previously shown that hypothalamic tissue can release IR-PRL in vitro when depolarized by potassium. In this study, we examined the release of IR-PRL from hypothalami obtained from intact and ovariectomized rats and incubated in the presence of veratridine (an alkaloid which depolarizes excitable membranes), angiotensin II, or thyrotropin-releasing hormone. Hypothalamic tissue spontaneously released IR-PRL, and this release was significantly increased by veratridine or angiotensin II in a dose-dependent manner. The specificity of the angiotensin-II-evoked IR-PRL release was demonstrated by the inhibitory effect of saralasin, an angiotensin II receptor antagonist, on hypothalamic IR-PRL release. Thyrotropin-releasing hormone (100-mu-M) had no effect on hypothalamic IR-PRL release. Ovariectomy decreased hypothalamic IR-PRL content and IR-PRL release in response to veratridine and angiotensin II. The effect of estradiol on hypothalamic IR-PRL content and release was also examined by obtaining hypothalami from ovariectomized rats injected with estradiol (1-mu-g/day) or vehicle for 5 days. When compared with vehicle injected rats, administration of estradiol significantly increased the hypothalamic IR-PRL content (46 +/- 4 vs. 81 +/- 16 ng/mg protein). In the same rats, the veratridine (100 mM; 7.26 +/- 0.97 vs. 10.4 +/- 1.46 ng/ml) and angiotensin II (1-mu-M; 5.08 +/- 0.84 vs. 9.9 +/- 1.2 ng/ml) stimulated IR-PRL release was significantly increased when compared with vehicle-injected rats. These data indicate that angiotensin II, but not thyrotropin-releasing hormone, stimulates the release of IR-PRL from the female hypothalamus. The increase in hypothalamic IR-PRL content and release by estradiol suggests that estradiol stimulates the hypothalamic IR-PRL synthesis, resulting in an increase in the releasable pool of IR-PRL.