OVARIAN BETA-ADRENERGIC RECEPTORS DURING THE ONSET OF PUBERTY - CHARACTERIZATION, DISTRIBUTION, AND COUPLING TO STEROIDOGENIC RESPONSES
OVARIAN BETA-ADRENERGIC RECEPTORS DURING THE ONSET OF PUBERTY - CHARACTERIZATION, DISTRIBUTION, AND COUPLING TO STEROIDOGENIC RESPONSES
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DOI：
10.1210/endo-110-4-1124
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发表时间：
1982-01-01
期刊：
影响因子：
4.8
通讯作者：
OJEDA, SR
中科院分区：
文献类型：
--
作者：
AGUADO, LI;PETROVIC, SL;OJEDA, SR
在一项试图研究肾上腺素能机制参与控制[大鼠]青春期卵巢功能的研究中，β的存在。-肾上腺素能受体存在于青春期前和青春期周围的卵巢中。以[125I]碘羟基苄基平多洛尔（IHBP）为配体，获得了一类高亲和、低容量的单体。颗粒细胞和残余卵巢均可见-肾上腺素能区。饱和度曲线的Scatchard图分析或结合曲线的动力学分析为配体-受体结合提供了相同的平衡Kd值。解离实验表明，与受体结合的配体既有松散结合、易置换的成分，也有紧密结合、不可置换的成分。l -普萘洛尔[抑制常数(Ki) = 10.5 nM]、异丙肾上腺素（Ki = 696 nM）和zinterol （a. beta）均能抑制IHBP的结合。2-肾上腺素能激动剂（Ki = 187 nM）。美托洛尔，一种β。1-拮抗剂表现出更高的Ki （5.3 μ m）。结合参数的计算机分析表明，> 99%的结合位点为。β。在发情期和发情后期，颗粒细胞和残留卵巢中受体含量显著增加。全卵巢受体含量在发情期和发情后期显著增加。全卵巢受体含量在发情至发情晚期上午期间显著升高，在第1次LH高峰时下降，在发情期间保持较低水平，在第1次发情当天显著升高。在青春期的各个阶段，受体亲和力基本相同（IHBP的Kd = 0.1-0.2 nM）。用zinterol， a. β在青春期周围卵巢孵化。2-肾上腺素能激动剂，诱导黄体酮从早发情卵巢和晚发情卵巢释放，但不从无发情卵巢释放。排卵后，即在发情和发情第1天的动物中，观察到黄体酮反应显着增加。Zinterol诱导雄烯二酮在青春期的所有阶段释放，但诱导睾酮仅在早期和晚期卵巢释放。在研究的青春期的任何阶段，激动剂都不能显著增加雌二醇的释放。未成熟的卵巢可能含有一群β细胞。-肾上腺素能部位。类型，这些受体的刺激似乎引起类固醇释放，以不同的方式，在第一次排卵的日子里。研究发现，对- β的类固醇反应。2-肾上腺素能刺激是在青春期的早期发情阶段产生的。-受体含量和孕酮反应在第一次排卵后增加，表明肾上腺素能机制参与了成人卵巢功能的启动。
In an attempt to study the involvement of an adrenergic mechanism in the control of [rat] ovarian function at puberty, the presence of .beta.-adrenergic receptors was demonstrated, and the receptors were characterized in pre- and peripubertal ovaries. Using [125I]iodohydroxybenzylpindolol (IHBP) as a ligand, a single class of high affinity, low capacity .beta.-adrenergic sites was found in both granulosa cells and residual ovary. Analysis of Scatchard plots derived from saturation curves or kinetic analysis of association curves provided identical equilibrium Kd values for the ligand-receptor binding. Dissociation experiments showed that the ligand binding to the receptor had the presence of both loosely bound, easily displaceable and tight, nondisplaceable components. IHBP binding was inhibited by L-propranolol [inhibition constant (Ki) = 10.5 nM], isoproterenol (Ki = 696 nM) and zinterol, a .beta.2-adrenergic agonist (Ki = 187 nM). Metoprolol, a .beta.1-antagonist, exhibited a much higher Ki (5.3 .mu.M). Computer analysis of the binding parameters indicated that > 99% of the binding sites were .beta.2. Receptor content in both granulosa cells and residual ovary increased significantly between the anestrous and the late proestrous phases of puberty. The receptor content of whole ovaries increased significantly between the anestrous and the late proestrous phases of puberty. The receptor content of whole ovaries increased significantly between anestrus and the morning of late proestrus, decreased at the time of the 1st LH surge, remained low during estrus, and increased strikingly on the day of 1st diestrus. In all pubertal stages, receptor affinity appeared to be essentially the same (Kd for IHBP = 0.1-0.2 nM). Incubation of peripubertal ovaries with zinterol, a .beta.2-adrenergic agonist, induced progesterone release from early proestrous and late proestrous ovaries, but not from anestrous ovaries. A marked increase in progesterone response was observed after ovulation, i.e., in estrous and diestrous day 1 animals. Zinterol induced androstenedione release at all pubertal phases, but elicited testosterone release only from early proestrous and late proestrous ovaries. The agonist failed to produce a significant increase in estradiol release at any phase of puberty studied. The immature ovary may contain a population of .beta.-adrenergic sites of the .beta.-type, and stimulation of these receptors appear to elicit steroid release, in a differential manner, during the days encompassing the 1st ovulation. The findings that a steroidogenic response to .beta.2-adrenergic stimulation develops during the early proestrous phase of puberty and that both the .beta.-receptor content and the progesterone response increase after the 1st ovulation suggest the involvement of an adrenergic mechanism in the initiation of adult ovarian function.