Activation of ovarian sympathetic nerves in polycystic ovary syndrome.
Activation of ovarian sympathetic nerves in polycystic ovary syndrome.
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DOI：
10.1210/endo.133.6.7902268
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发表时间：
1993-12
期刊：
影响因子：
4.8
通讯作者：
H. Lara;J. Ferruz;S. Luza;D. Bustamante;Y. Borges;S. Ojeda
中科院分区：
文献类型：
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作者：
H. Lara;J. Ferruz;S. Luza;D. Bustamante;Y. Borges;S. Ojeda
多囊卵巢综合征（PCOS）是影响育龄妇女最常见的卵巢疾病之一。尽管广泛的调查，多囊卵巢综合征的病因仍然知之甚少。实验表明，单剂量长效雌激素戊酸雌二醇（estradiol valerate， EV）可诱导啮齿动物出现pco样综合征。我们已经使用这个模型来检查多囊卵巢综合征与卵巢交感神经控制紊乱有关的可能性。卵巢神经末梢对腺体跨壁刺激的新合并去甲肾上腺素（NE）释放在囊肿形成前（注射EV后30天）显著增加，并在囊肿形成时（60天）保持升高。引起的NE释放增加伴随着NE含量的增加和[3H]NE进入卵巢组织的增强；这两种变化都是在EV治疗后30天开始的，在囊肿形成时变得明确。儿茶酚胺稳态改变提示卵巢交感神经流出量总体增加，并伴有鞘细胞间质组织β -肾上腺素能受体选择性下调；在这些交感神经支配的卵巢腔室中，β -肾上腺素能受体的浓度在PCO中明显低于发情周期的发情期，在发情期，β -肾上腺素能受体的浓度在正常卵巢周期中达到最低水平。酪氨酸羟化酶活性仅在每毫克卵巢中表达时才增加，而不是绝对量（即每总卵巢），这表明酶活性受到儿茶酚胺含量增加的调节。结果表明，卵巢交感神经的激活先于卵巢囊肿的形成，并提出卵巢交感神经输入紊乱可能导致多囊卵巢的病因。
Polycystic ovarian syndrome (PCOS) is one of the most common human ovarian pathologies affecting women of reproductive age. Despite extensive investigation, the etiology of PCOS remains poorly understood. Experimentally, a PCO-like syndrome can be induced in rodents by a single dose of the long-acting estrogen, estradiol valerate (EV). We have used this model to examine the possibility that PCOS is associated with derangement of the sympathetic control of the ovary. The release of newly incorporated norepinephrine (NE) from ovarian nerve terminals in response to transmural stimulation of the gland increased significantly before the formation of cysts (30 days after EV injection) and remained elevated at the time when cysts form (60 days). The increase in evoked NE release was accompanied by an augmented NE content and enhanced incorporation of [3H]NE into ovarian tissue; both of these changes had been initiated by 30 days after EV treatment and became unambiguous at the time of cyst formation. The overall increase in ovarian sympathetic outflow suggested by these alterations in catecholamine homeostasis was accompanied by a thecal cell-interstitial tissue selective down-regulation of beta-adrenergic receptors; the beta-adrenergic receptor concentration in these sympathetically innervated ovarian compartments was significantly lower in PCO than during the estrous phase of the estrous cycle, a time at which the beta-adrenergic receptor concentration reaches its lowest levels in normal cycling ovaries. Tyrosine hydroxylase activity was found to increase only when expressed per mg ovary, but not in absolute terms (i.e. per total ovary), suggesting regulation of enzyme activity by the enhanced catecholamine content. The results demonstrate that an activation of the sympathetic neurons innervating the ovary precedes the development of cysts in EV-induced PCOS and raise the possibility that a derangement of sympathetic inputs to the ovary contributes to the etiology of PCOS.