Rondeel J M, de Greef W J, van der Schoot P, Karels B, Klootwijk W, Visser T J
Department of Endocrinology, Growth and Reproduction, Medical Faculty, Erasmus University, Rotterdam, The Netherlands.
Endocrinology. 1988 Jul;123(1):523-7. doi: 10.1210/endo-123-1-523.
TRH is a potent stimulator of pituitary TSH release, but its function in the physiological regulation of thyroid activity is still controversial. The purpose of the present study was to investigate TRH and catecholamine secretion into hypophysial portal blood of hypothyroid and hyperthyroid rats, and in rats bearing paraventricular area lesions. Male rats were made hypothyroid with methimazole (0.05% in drinking water) or hyperthyroid by daily injections with T4 (10 micrograms/100 g BW). Untreated male rats served as euthyroid controls. On day 8 of treatment they were anesthetized to collect peripheral and hypophysial stalk blood. In euthyroid, hypothyroid and hyperthyroid rats plasma T3 was 1.21 +/- 0.04, 0.60 +/- 0.04, and 7.54 +/- 0.33 nmol/liter, plasma T4 50 +/- 3, 16 +/- 2, and 609 +/- 74 nmol/liter, and plasma TSH 1.58 +/- 0.29, 8.79 +/- 1.30, and 0.44 +/- 0.03 ng RP-2/ml, respectively. Compared with controls, hyperthyroidism reduced hypothalamic TRH release (0.8 +/- 0.1 vs. 1.5 +/- 0.2 ng/h) but was without effect on catecholamine release. Hypothyroidism did not alter TRH release, but the release of dopamine increased 2-fold and that of noradrenaline decreased by 20%. Hypothalamic TRH content was not affected by the thyroid status, but dopamine content in the hypothalamus decreased by 25% in hypothyroid rats. Twelve days after placement of bilateral electrolytic lesions in the paraventricular area plasma thyroid hormones and TSH levels were lower than in control rats (T3: 0.82 +/- 0.05 vs. 1.49 +/- 0.07 nmol/liter; T4: 32 +/- 4 vs. 66 +/- 3 nmol/liter; TSH: 1.08 +/- 0.17 vs. 3.31 +/- 0.82 ng/ml). TRH release in stalk blood in rats with lesions was 15% of that of controls, whereas dopamine and adrenaline release had increased by 50% and 40%, respectively. These results suggest that part of the feedback action of thyroid hormones is exerted at the level of the hypothalamus. Furthermore, TRH seems an important drive for normal TSH secretion by the anterior pituitary gland, and thyroid hormones seem to affect the hypothalamic release of catecholamines.
促甲状腺激素释放激素(TRH)是垂体促甲状腺激素(TSH)释放的强效刺激物,但其在甲状腺活动生理调节中的作用仍存在争议。本研究的目的是调查甲状腺功能减退和甲状腺功能亢进大鼠以及患有室旁区域损伤的大鼠垂体门脉血中TRH和儿茶酚胺的分泌情况。雄性大鼠用甲巯咪唑(饮用水中含0.05%)制成甲状腺功能减退模型,或通过每日注射T4(10微克/100克体重)制成甲状腺功能亢进模型。未治疗的雄性大鼠作为甲状腺功能正常的对照。在治疗第8天,将它们麻醉以采集外周血和垂体柄血。甲状腺功能正常、减退和亢进的大鼠血浆T3分别为1.21±0.04、0.60±0.04和7.54±0.33纳摩尔/升,血浆T4分别为50±3、16±2和609±74纳摩尔/升,血浆TSH分别为1.58±0.29、8.79±1.30和0.44±0.03纳克RP - 2/毫升。与对照组相比,甲状腺功能亢进降低了下丘脑TRH释放(0.8±0.1对1.5±0.2纳克/小时),但对儿茶酚胺释放无影响。甲状腺功能减退未改变TRH释放,但多巴胺释放增加了2倍,去甲肾上腺素释放减少了20%。下丘脑TRH含量不受甲状腺状态影响,但甲状腺功能减退大鼠下丘脑多巴胺含量降低了25%。在室旁区域放置双侧电解损伤12天后,血浆甲状腺激素和TSH水平低于对照大鼠(T3:0.82±0.05对1.49±0.07纳摩尔/升;T4:32±4对66±3纳摩尔/升;TSH:1.08±0.17对3.31±0.82纳克/毫升)。有损伤的大鼠垂体柄血中TRH释放量为对照大鼠的15%,而多巴胺和肾上腺素释放分别增加了50%和40%。这些结果表明甲状腺激素的部分反馈作用在下丘脑水平发挥。此外,TRH似乎是垂体前叶正常TSH分泌的重要驱动因素,甲状腺激素似乎影响下丘脑儿茶酚胺的释放。