Husain Jawadi M, Ho L, DeJong D C
Horm Res. 1984;19(2):91-6. doi: 10.1159/000179872.
Effect of thyrotropic releasing hormone (TRH) on plasma arginine vasopressin (AVP) was studied in human subjects. All 7 normal controls and 2 hypothyrotropic hypothyroid subjects failed to show any rise of AVP on TRH administration. The 4 primary hypothyroid subjects had elevated basal AVP level and showed further elevation on TRH administration. Our data suggests that elevated TRH in primary hypothyroid subjects may act directly as a nonosmotic stimulus or modulate the osmoreceptor and hypothalamic neurohypophyseal system for AVP release.
在人类受试者中研究了促甲状腺激素释放激素(TRH)对血浆精氨酸加压素(AVP)的影响。所有7名正常对照者和2名促甲状腺激素分泌不足的甲状腺功能减退受试者在给予TRH后均未出现AVP升高。4名原发性甲状腺功能减退受试者的基础AVP水平升高,给予TRH后进一步升高。我们的数据表明,原发性甲状腺功能减退受试者中升高的TRH可能直接作为一种非渗透性刺激,或调节渗透压感受器和下丘脑神经垂体系统以释放AVP。