肾上腺素能拮抗剂对短期卵巢切除类固醇大鼠LH激增的影响。

W P Pi
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引用次数: 0

摘要

研究了肾上腺素能刺激对短期去卵巢大鼠卵巢类固醇激素诱导的促黄体生成素(LH)释放的影响。雌性Sprague-Dawley大鼠在发情第1天约1000 h进行OVX。切除卵巢后,立即给大鼠植入含雌二醇的硅橡胶胶囊,并植入心房硅橡胶管进行频繁采血。所有大鼠均于次日上午9时30分给予孕酮s.c. 2 mg。在1200小时,大鼠接受额外的治疗:生理盐水,哌唑嗪HC1 (α 1-肾上腺素能拮抗剂),育亨宾HC1 (α 2-肾上腺素能拮抗剂),或普萘洛尔HC1 (β -肾上腺素能拮抗剂)s.c。两种不同剂量的肾上腺素能拮抗剂在等摩尔的基础上使用,以显示它们对类固醇诱导的黄体生成素分泌的有效性。分别于治疗前、治疗后1、3、5小时通过留置管采集血样。吡唑嗪和育亨宾可抑制/延缓卵巢类固醇诱导的黄体生成素激增,而心得安可增强黄体生成素激增,并呈剂量依赖性。结果表明,下丘脑α 1-、α 2-和β肾上腺素受体参与了短期注射ovx类固醇大鼠LH激增的控制。主要是α 1-和α 2-肾上腺素受体在调节卵巢类固醇诱导的LH激增中起促进作用,β -肾上腺素受体起抑制作用。
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Effects of adrenergic antagonists on LH surge in short-term ovariectomized-steroids-primed rats.

Characterization of adrenergic stimuli on luteinizing hormone (LH) release induced by ovarian steroids in short-term ovariectomized (OVX) rats was studied. Female Sprague-Dawley rats were OVX about 1000 h on the diestrous day 1. After ovariectomy, rats were immediately inserted estradiol-containing Silastic capsules s.c. and implanted atrial Silastic tubing for frequent blood samplings. All the rats received 2 mg of progesterone s.c. at 0930 h the next morning. At 1200 h, the rats received additional treatments: a saline vehicle, prazosin HC1 (an alpha 1-adrenergic antagonist), yohimbine HC1 (an alpha 2-adrenergic antagonist), or propranolol HC1 (a beta-adrenergic antagonist) s.c., respectively. Two different doses of individual adrenergic antagonists were used on an equimolar basis in order to show their effectiveness on steroids-induced LH secretion. Blood samples were collected before and 1, 3, and 5 hours after the treatments through indwelt tubings. LH surge induced by ovarian steroids was suppressed/delayed by prazosin and yohimbine, but potentiated by propranolol in a dose-dependent manner. Results suggested that the hypothalamic alpha 1-, alpha 2-, and beta-adrenoreceptors were involved in the control of LH surge in the short-term OVX-steroids-primed rats. Principally, the alpha 1- and alpha 2-adrenoreceptors played a facilitatory role, and the beta-adrenoreceptors played an inhibitory role in the regulation of LH surge induced by ovarian steroids.

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