Del Rio G, Zizzo G, Marrama P, Venneri M G, Della Casa L, Velardo A
Department of Endocrinology and Metabolism, University of Modena, Italy.
Clin Endocrinol (Oxf). 1994 Feb;40(2):235-9. doi: 10.1111/j.1365-2265.1994.tb02474.x.
Several studies indicate an inverse relationship between the sympathetic nervous system activity and thyroid function. Altered adrenoceptor sensitivity, particularly alpha 1 and beta, have been described in hypothyroid and hyperthyroid patients. No information in patients with thyroid disease is available on the main mechanism regulating sympathetic nervous system outflow, i.e. the alpha 2-adrenoceptor pathway. In our study we evaluated alpha 2-adrenergic activity in patients with thyroid disease by the assessment of cardiovascular and catecholamine response to clonidine, a central alpha 2 adrenergic agonist.
Ten patients with hypothyroidism, six patients with hyperthyroidism before and during adequate therapy, and ten healthy subjects.
After three blood samples for the basal determination of noradrenaline and adrenaline, the subjects swallowed 4 micrograms/kg body weight of clonidine. Blood pressure and pulse rate were measured 30, 60, 90, 120, 130 and 140 minutes after clonidine administration; blood samples for determination of catecholamines were drawn at 120, 130 and 140 minutes.
At presentation the decrease in plasma noradrenaline after clonidine in the patients was similar to that of the control group (hypothyroids: 1.07 +/- 0.23 nmol/l mean +/- SEM; hyperthyroids: 0.54 +/- 0.06 nmol/l; controls; 0.36 +/- 0.10 nmol/l; F = 1.2, P = NS). No differences were detected in the fall in adrenaline and mean arterial pressure (MAP) after clonidine. The adequate therapy induced in hypothyroid patients a decrease in the basal levels of noradrenaline (1.88 +/- 0.28 vs 0.67 +/- 0.10 nmol/l; P < 0.05) and a lesser fall in mean arterial pressure after clonidine (delta MAP 20.4 +/- 2.0 vs 9.7 +/- 2.8 mmHg; P < 0.05). No variations were detected in hyperthyroid patients after therapy either in basal hormones levels or in the magnitude of decrement in MAP and noradrenaline induced by clonidine.
We conclude that in spite of the previously reported abnormalities in alpha 1 and beta-adrenergic receptor activity, the inhibitory alpha 2-receptor pathway is normal in patients with altered thyroid function.
多项研究表明交感神经系统活动与甲状腺功能之间存在负相关关系。在甲状腺功能减退和亢进患者中，已发现肾上腺素能受体敏感性发生改变，尤其是α1和β受体。目前尚无关于甲状腺疾病患者中调节交感神经系统传出的主要机制，即α2 - 肾上腺素能受体途径的相关信息。在我们的研究中，我们通过评估心血管系统及儿茶酚胺对可乐定（一种中枢α2肾上腺素能激动剂）的反应，来评估甲状腺疾病患者的α2肾上腺素能活性。
10例甲状腺功能减退患者、6例甲亢患者（治疗前及充分治疗期间）以及10名健康受试者。
在采集三份血样用于基础去甲肾上腺素和肾上腺素测定后，受试者口服4微克/千克体重的可乐定。在服用可乐定后30、60、90、120、130和140分钟测量血压和脉搏率；在120、130和140分钟采集血样用于测定儿茶酚胺。
就诊时，患者服用可乐定后血浆去甲肾上腺素的下降幅度与对照组相似（甲状腺功能减退患者：1.07±0.23纳摩尔/升，均值±标准误；甲亢患者：0.54±0.06纳摩尔/升；对照组：0.36±0.10纳摩尔/升；F = 1.2，P = 无显著性差异）。服用可乐定后肾上腺素下降幅度及平均动脉压（MAP）未检测到差异。甲状腺功能减退患者的充分治疗导致基础去甲肾上腺素水平下降（1.88±0.28对0.67±0.10纳摩尔/升；P < 0.05），且服用可乐定后平均动脉压下降幅度较小（MAP变化值20.4±2.0对9.7±2.8毫米汞柱；P < 0.05）。甲亢患者治疗后，基础激素水平、可乐定诱导的MAP和去甲肾上腺素下降幅度均未检测到变化。
我们得出结论，尽管先前报道了α1和β肾上腺素能受体活性存在异常，但甲状腺功能改变患者的抑制性α2受体途径是正常的。
