Elias A N, Vaziri N D, Pandian M R, Iyer K, Ansari M A
Department of Medicine, University of California at Irvine Medical Center, Orange.
Neuroendocrinology. 1988 Mar;47(3):181-5. doi: 10.1159/000124911.
The role of endogenous opioids in the control of thyroid-stimulating hormone (TSH) 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 altered TSH secretion in uremia, we also studied a group of normal control animals who were pair-fed with the uremic animals, so that their weights were comparable to that of the uremic animals. Naloxone administration produced a significant increase in the basal concentration of TSH response to TRH (5 micrograms i.v.) was significantly blunted in the uremic animals compared to the normal controls and the starved animals. Naloxone administration did not alter the peak thyrotropin-releasing hormone (TRH) stimulated TSH response in any of the experimental groups of rats. Because of the possibility that the effects of naloxone on TSH secretion in the uremic rats were related to impaired clearance of the naloxone in those animals, an additional group of normal rats was given twice the dose of naloxone administered to the uremic animals. The higher dose of naloxone was similarly without effect on the basal or TRH-stimulated TSH secretion in this group. The data suggest that experimental renal failure is associated with diminished sensitivity of the thyrotroph to TRH stimulation and that this blunted sensitivity cannot be abolished by blockade of endogenous opioids by naloxone. Opioid blockade does, however, increase basal TSH secretion in uremic animals, suggesting an increase in endogenous opioidergic tone in uremia.(ABSTRACT TRUNCATED AT 250 WORDS)
使用麻醉拮抗剂纳洛酮研究了内源性阿片类物质在控制尿毒症雄性大鼠促甲状腺激素（TSH）分泌中的作用。为了消除尿毒症引起的厌食导致体重减轻对尿毒症时TSH分泌改变的影响，我们还研究了一组与尿毒症动物配对喂养的正常对照动物，以使它们的体重与尿毒症动物相当。与正常对照动物和饥饿动物相比，尿毒症动物静脉注射5微克促甲状腺激素释放激素（TRH）后，纳洛酮给药使TSH反应的基础浓度显著升高，而尿毒症动物对TRH的反应明显减弱。纳洛酮给药未改变任何实验组大鼠促甲状腺激素释放激素（TRH）刺激的TSH峰值反应。由于纳洛酮对尿毒症大鼠TSH分泌的影响可能与这些动物中纳洛酮清除受损有关，另一组正常大鼠给予了两倍于尿毒症动物的纳洛酮剂量。该组中较高剂量的纳洛酮对基础或TRH刺激的TSH分泌同样没有影响。数据表明，实验性肾衰竭与促甲状腺细胞对TRH刺激的敏感性降低有关，并且这种减弱的敏感性不能通过纳洛酮阻断内源性阿片类物质来消除。然而，阿片类物质阻断确实增加了尿毒症动物的基础TSH分泌，表明尿毒症时内源性阿片能张力增加。（摘要截断于250字）
