促甲状腺激素释放激素抑制大鼠肾上腺皮质的糖皮质激素分泌：体内和体外研究

Thyrotropin-releasing hormone inhibits glucocorticoid secretion of rat adrenal cortex: in vivo and in vitro studies.

作者信息

Neri G, Malendowicz L K, Andreis P, Nussdorfer G G

机构信息

Department of Anatomy, University of Padua, Italy.

出版信息

Endocrinology. 1993 Aug;133(2):511-4. doi: 10.1210/endo.133.2.8393765.

DOI:10.1210/endo.133.2.8393765

PMID:8393765

Abstract

The bolus iv administration of TRH dose-dependently decreased ACTH-enhanced plasma corticosterone (B) concentration in rats, without affecting the basal one. The effects of TRH on steroid secretion of dispersed rat inner adrenocortical cells were investigated by HPLC. TRH significantly decreased both basal and ACTH-stimulated post-11-deoxycorticosterone (DOC) secretion (i.e. 18-hydroxy-DOC and B) and concomitantly raised DOC and progesterone release, so that the total postpregnenolone yield of our preparations was unaffected. TRH did not alter either basal or ACTH-stimulated pregnenolone production by isolated rat adrenocortical cells. It was concluded that TRH is an inhibitor of glucocorticoid secretion in rats, which electively impairs the late steps of B synthesis (i.e. 11- and 18-hydroxylation) without affecting the earlier steps, including the rate-limiting one of this process.

摘要

静脉推注促甲状腺激素释放激素（TRH）能使大鼠体内促肾上腺皮质激素（ACTH）增强的血浆皮质酮（B）浓度呈剂量依赖性降低，而对基础浓度无影响。采用高效液相色谱法（HPLC）研究了TRH对分散的大鼠肾上腺皮质内层细胞类固醇分泌的影响。TRH显著降低基础状态及ACTH刺激后的11-脱氧皮质酮（DOC）分泌（即18-羟脱氧皮质酮和B），同时提高DOC和孕酮的释放，因此我们制备物中孕烯醇酮的总产后产量未受影响。TRH对分离的大鼠肾上腺皮质细胞基础状态或ACTH刺激后的孕烯醇酮生成均无改变。研究得出结论，TRH是大鼠糖皮质激素分泌的抑制剂，它选择性损害B合成的后期步骤（即11-羟化和18-羟化），而不影响包括该过程限速步骤在内的早期步骤。