甲状腺激素可调节大鼠垂体前叶中肌醇磷酸的形成，以响应促甲状腺激素释放激素。

Thyroid hormones regulate the formation of inositol phosphate in response to thyrotropin-releasing hormone in rat anterior pituitaries.

作者信息

Iriuchijima T, Michimata T, Miyashita K, Ogiwara T, Yamada M, Murakami M, Mori M

机构信息

First Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.

出版信息

Neuropeptides. 1992 Jan;21(1):49-53. doi: 10.1016/0143-4179(92)90151-l.

DOI:10.1016/0143-4179(92)90151-l

PMID:1738433

Abstract

The effects of thyroid hormones on TSH secretion and inositol phospholipid hydrolysis in response to thyrotropin-releasing hormone (TRH) in rat anterior pituitaries were examined. Experimental hypothyroidism caused a significant increase in [3H]inositol phosphate ([3H]IP) formation in response to TRH in rat anterior pituitaries with a concomitant elevation of blood TSH. In contrast, administration of thyroxine (T4) to hypothyroid rats resulted in a complete restoration of blood TSH and TRH-stimulated [3H]IP formation to the euthyroid control value. Furthermore, in vitro pre-treatment of anterior pituitaries with triiodothyronine (T3) produced a dose-dependent decrease in both TSH secretion and the formation of [3H]IP in response to TRH. These results indicate that thyroid hormones regulate TRH receptor-linked inositol phospholipid hydrolysis in the rat anterior pituitary, suggesting that negative feedback action of thyroid hormone occurs at post receptor event in the rat anterior pituitary, which may, to a certain extent, be responsible for the underlying mechanism of T3 inhibition of TSH secretion.

摘要

研究了甲状腺激素对大鼠垂体前叶促甲状腺激素（TSH）分泌以及对促甲状腺激素释放激素（TRH）反应中肌醇磷脂水解的影响。实验性甲状腺功能减退导致大鼠垂体前叶对TRH反应的[3H]肌醇磷酸（[3H]IP）生成显著增加，同时血TSH升高。相反，给甲状腺功能减退大鼠施用甲状腺素（T4）可使血TSH和TRH刺激的[3H]IP生成完全恢复到正常甲状腺功能对照值。此外，用三碘甲状腺原氨酸（T3）对垂体前叶进行体外预处理，可使TSH分泌和对TRH反应的[3H]IP生成呈剂量依赖性降低。这些结果表明，甲状腺激素调节大鼠垂体前叶TRH受体相关的肌醇磷脂水解，提示甲状腺激素的负反馈作用发生在大鼠垂体前叶的受体后事件，这可能在一定程度上是T3抑制TSH分泌的潜在机制。