Elias A N, Vaziri N D, Panadian M R, Iyer K, Ansari M A, Yazdani M
Department of Medicine, University of California, Irvine.
Horm Res. 1988;30(1):39-43. doi: 10.1159/000181024.
The role of endogenous opioids in the control of gonadotropin secretion in uremic male rats was investigated using the narcotic antagonist, naloxone. In order to eliminate the effect of weight loss due to uremia-induced anorexia as a cause of previously described altered gonadotropin secretion in uremia, we also studied a group of normal pair-fed control animals who exhibited a weight loss comparable to that of the uremic animals. Naloxone administration had no effect on the basal or LRH-stimulated peak concentrations of LH and FSH in the normal or the uremic rats. Basal and LRH-stimulated gonadotropin responses in the pair-fed rats were comparable to those seen in the normal rats. Similarly, opioid blockade produced no change in the basal or LRH-stimulated gonadotropin responses in the pair-fed animals. Testosterone concentrations were significantly lower in the uremic and pair-fed animals compared to the normal rats. The data suggest that experimental renal failure is not associated with altered opioidergic tone, as it relates to gonadotropin secretion, or to diminished sensitivity of the gonadotroph to LRH stimulation. The decreased testosterone concentration seen in the uremic and pair-fed rats may reflect abnormalities in gonadal hormone secretion due to primary pathology occurring at the level of the gonad. These abnormalities may be reflected as diminished Leydig cell sensitivity to LH. The inappropriately low concentrations of LH in the presence of low testosterone together with normal gonadotropin response to exogenous LRH also suggest an abnormal secretion of endogenous LRH. It is not clear whether this presumed abnormality in LRH secretion is a primary event or is related to decreased testosterone production by the testes in the uremic and pair-fed rats.
使用麻醉拮抗剂纳洛酮研究了内源性阿片类物质在尿毒症雄性大鼠促性腺激素分泌控制中的作用。为了消除尿毒症引起的厌食导致体重减轻对先前描述的尿毒症中促性腺激素分泌改变的影响，我们还研究了一组正常的配对喂养对照动物，它们的体重减轻程度与尿毒症动物相当。给予纳洛酮对正常或尿毒症大鼠的促黄体生成素（LH）和促卵泡生成素（FSH）的基础或促性腺激素释放激素（LRH）刺激的峰值浓度没有影响。配对喂养大鼠的基础和LRH刺激的促性腺激素反应与正常大鼠相当。同样，阿片类物质阻断对配对喂养动物的基础或LRH刺激的促性腺激素反应没有改变。与正常大鼠相比，尿毒症和配对喂养动物的睾酮浓度显著降低。数据表明，实验性肾衰竭与阿片能张力改变无关，因为它与促性腺激素分泌有关，也与促性腺细胞对LRH刺激的敏感性降低无关。尿毒症和配对喂养大鼠中观察到的睾酮浓度降低可能反映了性腺水平原发性病理导致的性腺激素分泌异常。这些异常可能表现为睾丸间质细胞对LH的敏感性降低。在睾酮水平低的情况下LH浓度异常低，同时促性腺激素对外源性LRH反应正常，这也表明内源性LRH分泌异常。目前尚不清楚这种推测的LRH分泌异常是原发性事件还是与尿毒症和配对喂养大鼠睾丸睾酮产生减少有关。
