Fommei Enza, Iervasi Giorgio
National Council of Research, University of Pisa, Italy.
J Clin Endocrinol Metab. 2002 May;87(5):1996-2000. doi: 10.1210/jcem.87.5.8464.
Arterial hypertension is known to be frequently associated with thyroid dysfunction, with a particularly high prevalence in chronic hypothyroidism. However, to our knowledge no comprehensive study addressed causal mechanisms possibly involved in this association. We here report the physiological relationships between blood pressure and neuro-humoral modifications induced by acute hypothyroidism in normotensive subjects. Twelve normotensive patients with previous total thyroidectomy were studied. Ambulatory 24-h blood pressure monitoring was performed, and free T(3), free T(4), TSH, PRA, aldosterone, cortisol, adrenaline, and noradrenaline were assayed 6 wk after oral L-T(4) withdrawal (phase 1) and 2 months after resumption of treatment (phase 2). During the hypothyroid state (TSH, 68.1 +/- 27.7 microIU/ml; mean +/- SD), daytime arterial systolic levels slightly, but significantly, increased (125.5 +/- 9.7 vs. 120.4 +/- 10.8 mm Hg; P < 0.05), and daytime diastolic levels (84.6 +/- 7.9 vs. 76.4 +/- 6.8 mm Hg; P < 0.001), noradrenaline (2954 +/- 1578 vs. 1574 +/- 962 pmol/liter; P < 0.001), and adrenaline (228.4 +/- 160 vs. 111.3 +/- 46.1 pmol/liter; P < 0.05) also increased. PRA remained unchanged (0.49 +/- 0.37 vs. 0.35 +/- 0.21 ng/ml.h; P = NS), whereas both aldosterone (310.3 +/- 151 vs. 156.9 +/- 67.5 pmol/liter; P < 0.005) and cortisol (409.2 +/- 239 vs. 250.9 +/- 113 pmol/liter; P < 0.02) significantly increased. By using univariate logistic regression daytime arterial diastolic values, noradrenaline and aldosterone were found to be significantly related to the hypothyroid state (P < 0.02, P < 0.036, and P < 0.024, respectively). In conclusion, our data show that thyroid hormones participate in the control of systemic arterial blood pressure homeostasis in normotensive subjects. The observed sympathetic and adrenal activation in hypothyroidism, which is reversible with thyroid hormone treatment, may also contribute to the development of arterial hypertension in human hypothyroidism.
众所周知，动脉高血压常与甲状腺功能障碍相关，在慢性甲状腺功能减退症中患病率尤其高。然而，据我们所知，尚无全面研究探讨可能参与这种关联的因果机制。我们在此报告正常血压受试者急性甲状腺功能减退症引起的血压与神经 - 体液改变之间的生理关系。研究了12例既往接受过甲状腺全切术的正常血压患者。进行了24小时动态血压监测，并在口服左甲状腺素（L-T4）停药6周后（阶段1）和恢复治疗2个月后（阶段2）测定了游离T3、游离T4、促甲状腺激素（TSH）、肾素活性（PRA）、醛固酮、皮质醇、肾上腺素和去甲肾上腺素。在甲状腺功能减退状态下（TSH，68.1±27.7微国际单位/毫升；均值±标准差），白天动脉收缩压水平略有但显著升高（125.5±9.7对120.4±10.8毫米汞柱；P<0.05），白天舒张压水平（84.6±7.9对76.4±6.8毫米汞柱；P<0.001）、去甲肾上腺素（2954±1578对1574±962皮摩尔/升；P<0.001）和肾上腺素（228.4±160对111.3±46.1皮摩尔/升；P<0.05）也升高。PRA保持不变（0.49±0.37对0.35±0.21纳克/毫升·小时；P=无显著性差异），而醛固酮（310.3±151对156.9±67.5皮摩尔/升；P<0.005）和皮质醇（409.2±239对250.9±113皮摩尔/升；P<0.02）均显著升高。通过单因素逻辑回归分析发现，白天动脉舒张压值、去甲肾上腺素和醛固酮与甲状腺功能减退状态显著相关（分别为P<0.02、P<0.036和P<0.024）。总之，我们的数据表明甲状腺激素参与正常血压受试者全身动脉血压稳态的控制。在甲状腺功能减退症中观察到的交感神经和肾上腺激活，经甲状腺激素治疗可逆转，这也可能导致人类甲状腺功能减退症中动脉高血压的发生。
