Knigge U, Thuesen B, Wollesen F, Dejgaard A, Christiansen P M
J Clin Endocrinol Metab. 1984 Apr;58(4):692-7. doi: 10.1210/jcem-58-4-692.
GH responses to TRH occur in patients with certain diseases, such as acromegaly, severe liver disease, uremia, and mental disorders, and presumably reflect disruption of normal hypothalamic control of GH secretion. Since histamine (HA) inhibits hypothalamic stimulation of GH secretion, we investigated the combined effect of HA receptor activation and TRH administration on GH secretion in normal men. Eight men were given 4-h infusions of the following: saline, HA, HA plus mepyramine (Me; and H1-antagonist), HA plus cimetidine (C; an H2-antagonist), and C alone. TRH (200 micrograms) was injected iv 2 h after the start of each infusion. HA alone or in combination with either antagonist had no effect on basal or TRH-stimulated TSH secretion and no effect on basal GH secretion. However, when TRH was injected during H1 stimulation by HA plus C, GH secretion increased significantly [from 0.7 +/- 0.1 to 7.1 +/- 1.8 (+/- SEM) ng/ml; P less than 0.01] in seven of eight subjects. This GH response was reproducible and did not occur when saline was administered instead of TRH. A smaller and delayed GH response to TRH occurred during infusions of HA alone (from 0.8 +/- 0.1 to 4.9 +/- 1.0 ng/ml; P less than 0.05). No effect of TRH on GH secretion occurred during the infusion of saline (1.2 +/- 0.3 ng/ml), HA plus Me (0.9 +/- 0.1 ng/ml), or C (2.2 +/- 1.0 ng/ml). There was a significant increase in GH secretion after cessation of the infusions of HA (from 3.4 +/- 1.1 to 7.5 +/- 2.2 ng/ml) and HA plus Me (from 0.8 +/- 0.1 to 5.1 +/- 1.8 ng/ml). This rebound in GH secretion might indicate an inhibitory effect of TRH during H2-receptor stimulation. This concept is supported by the significantly smaller GH response to TRH during HA infusion than during HA plus C infusion (P less than 0.01). The study indicates that H1-receptor stimulation induces a stimulatory effect of TRH on GH secretion in normal men and that H2-receptor stimulation possibly induces an inhibitory effect of TRH on GH secretion.
生长激素（GH）对促甲状腺激素释放激素（TRH）的反应见于某些疾病患者，如肢端肥大症、严重肝病、尿毒症和精神障碍患者，这可能反映了下丘脑对GH分泌的正常控制受到破坏。由于组胺（HA）抑制下丘脑对GH分泌的刺激作用，我们研究了HA受体激活与TRH给药联合作用对正常男性GH分泌的影响。8名男性接受了以下4小时的静脉输注：生理盐水、HA、HA加美吡拉敏（Me，一种H1拮抗剂）、HA加西咪替丁（C，一种H2拮抗剂）以及单独使用C。在每次输注开始2小时后静脉注射TRH（200微克）。单独使用HA或与任何一种拮抗剂联合使用对基础或TRH刺激的促甲状腺激素（TSH）分泌均无影响，对基础GH分泌也无影响。然而，当在HA加C刺激H1受体期间注射TRH时，8名受试者中有7名的GH分泌显著增加[从0.7±0.1增至7.1±1.8（±标准误）纳克/毫升；P<0.01]。这种GH反应具有可重复性，而当注射生理盐水代替TRH时则未出现。单独输注HA期间对TRH的GH反应较小且延迟（从0.8±0.1增至4.9±1.0纳克/毫升；P<0.05）。在输注生理盐水（1.2±0.3纳克/毫升）、HA加Me（0.9±0.1纳克/毫升）或C（2.2±1.0纳克/毫升）期间，TRH对GH分泌无影响。在停止输注HA（从3.4±1.1增至7.5±2.2纳克/毫升）和HA加Me（从0.8±0.1增至5.1±1.8纳克/毫升）后，GH分泌显著增加。GH分泌的这种反弹可能表明在H2受体刺激期间TRH具有抑制作用。HA输注期间对TRH的GH反应明显小于HA加C输注期间（P<0.01），这一观点得到了支持。该研究表明，H1受体刺激可诱导TRH对正常男性GH分泌产生刺激作用，而H2受体刺激可能诱导TRH对GH分泌产生抑制作用。
