Harris A R, Christianson D, Smith M S, Fang S L, Braverman L E, Vagenakis A G
J Clin Invest. 1978 Feb;61(2):441-8. doi: 10.1172/JCI108955.
The physiological role of thyrotropin-releasing hormone (TRH) in the regulation of thyrotropin (thyroid-stimulating hormone, TSH) and prolactin (Prl) secretion has been assumed but not proven. Stimulation of their release requires pharmacologic doses of TRH. Lesions of the hypothalamus usually induce an inhibition of TSH secretion and an increase in Prl. To determine whether TRH is essential for TSH and Prl secretion in the rat, 0.1 ml of TRH antiserum (TRH-Ab) or normal rabbit serum was administered to normal, thyroidectomized, cold-exposed, and proestrus rats through indwelling atrial catheter. Serum samples were obtained before and at frequent intervals thereafter. Serum TSH concentrations in normal, thyroidectomized, cold-exposed, and proestrus rats were not depressed in specimens obtained up to 24 h after injection of normal rabbit serum. In contrast, serum TSH was significantly decreased after the administration of TRH-Ab in all normal (basal, 41+/-8 muU/ml [mean+/-SE]; 30 min, 6+/-2; 45 min, 8+/-3; 75 min, 4+/-2); thyroidectomized (basal, 642+/-32 muU/ml; 30 min, 418+/-32; 60 min, 426+/-36; 120 min, 516+/-146); coldstressed (basal, 68+/-19 muU/ml; 30 min, 4+/-3; 180 min, 16+/-8); and proestrus (basal, 11 a.m., 57+/-10 muU/ml; 1 p.m., 20+/-3; 3 p.m., 13+/-4; 5 p.m., 19+/-3) rats. However, 0.1 ml of TRH-Ab had no effect on basal Prl concentrations in normal or thyroidectomized rats and did not prevent the Prl rise in rats exposed to cold (basal, 68+/-7 ng/ml; 15 min, 387+/-121; 30 min, 212+/-132; 60 min, 154+/-114), or the Prl surge observed on the afternoon of proestrus (basal 11 a.m., 23+/-2 ng/ml; 1 p.m., 189+/-55; 3 p.m., 1,490+/-260; 5 p.m., 1,570+/-286). These studies demonstrate that TRH is required for TSH secretion in the normal, cold-exposed and proestrus rat and contributes, at least in part, to TSH secretion in the hypothyroid rat, but is not required for Prl secretion in these states.
促甲状腺激素释放激素(TRH)在调节促甲状腺激素(甲状腺刺激激素,TSH)和催乳素(Prl)分泌中的生理作用已被假定,但尚未得到证实。刺激它们的释放需要药理剂量的TRH。下丘脑损伤通常会导致TSH分泌受到抑制以及Prl升高。为了确定TRH对大鼠TSH和Prl分泌是否必不可少,通过留置心房导管向正常、甲状腺切除、冷暴露和动情前期的大鼠注射0.1ml的TRH抗血清(TRH-Ab)或正常兔血清。在此之前及之后的频繁时间间隔采集血清样本。在注射正常兔血清后长达24小时采集的样本中,正常、甲状腺切除、冷暴露和动情前期大鼠的血清TSH浓度并未降低。相比之下,在所有正常(基础值,41±8μU/ml[平均值±标准误];30分钟,6±2;45分钟,8±3;75分钟,4±2)、甲状腺切除(基础值,642±32μU/ml;30分钟,418±32;60分钟,426±36;120分钟,516±146)、冷应激(基础值,68±19μU/ml;30分钟,4±3;180分钟,16±8)和动情前期(上午11点基础值,57±10μU/ml;下午1点,20±3;下午3点,13±4;下午5点,19±3)大鼠中,注射TRH-Ab后血清TSH显著降低。然而,0.1ml的TRH-Ab对正常或甲状腺切除大鼠的基础Prl浓度没有影响,也不能阻止冷暴露大鼠(基础值,68±7ng/ml;15分钟,387±121;30分钟,212±132;60分钟,154±114)的Prl升高,或动情前期下午观察到的Prl激增(上午11点基础值,23±2ng/ml;下午1点,189±55;下午3点,1490±260;下午5点,1570±286)。这些研究表明,TRH是正常、冷暴露和动情前期大鼠TSH分泌所必需的,并且至少部分地促成了甲状腺功能减退大鼠的TSH分泌,但在这些状态下不是Prl分泌所必需的。