Department of Internal Medicine, Santa Maria della Misericordia Hospital, via Tre Martiri 140, 45100 Rovigo, Italy.
Unit of Internal Medicine, General Hospital of Bassano, Vicenza, Italy.
Ann Endocrinol (Paris). 2011 Sep;72(4):296-303. doi: 10.1016/j.ando.2011.05.004. Epub 2011 Jul 21.
This review describes the pathogenic mechanisms of blood pressure (BP) regulation and long-term control in thyroid disorders. Variations from the euthyroid status affect virtually all physiological systems but the effects on the cardiovascular system are particularly pronounced. Thyroid disorders induce several hemodynamic changes leading to elevated BP as a consequence of their interaction with endothelial function, vascular reactivity, renal hemodynamic and renin-angiotensin system. However, in thyroid disorders, the regulation of BP and the development and maintenance of variable forms of arterial hypertension (HT) are different. Hyperthyroidism results in an increased endothelium-dependent responsiveness secondary to the shear stress induced by the hyperdynamic circulation, and contributes to reduce vascular resistance. Conversely, hypothyroidism is accompanied by a marked decrease in sensitivity to sympathetic agonists with an increase of peripheral vascular resistance and arterial stiffness. Furthermore in animal models, hypothyroidism reduces the endothelium-dependent and nitric oxide-dependent vasodilatation. HT due to thyroid disorders is usually reversible with achievement of euthyroidism, but in some cases pharmacological treatment for BP control is required. In hyperthyroidism, β-blockers are the first-choice treatment to control BP but when they are contraindicated or not tolerated, ACE-inhibitors or calcium-channel blockers (CCB) are recommended. Hypothyroidism is a typical low rennin HT form showing a better antihypertensive response to CCB and diuretics; indeed in hypothyroidism a low-sodium diet seems further to improve BP control. Randomized clinical trials to compare the efficacy on BP control of the antihypertensive treatment in thyroid disorders are needed.
这篇综述描述了甲状腺疾病中血压调节和长期控制的致病机制。从甲状腺功能正常状态的变化几乎会影响所有的生理系统，但对心血管系统的影响尤为显著。甲状腺疾病会引起多种血液动力学变化，导致血压升高，这是它们与内皮功能、血管反应性、肾脏血液动力学和肾素-血管紧张素系统相互作用的结果。然而，在甲状腺疾病中，血压的调节以及不同类型的动脉高血压（HT）的发展和维持是不同的。甲状腺功能亢进会导致内皮依赖性反应性增加，这是由高动力循环引起的切应力引起的，有助于降低血管阻力。相反，甲状腺功能减退伴有对外周血管阻力和动脉僵硬度增加的交感神经激动剂敏感性显著降低。此外，在动物模型中，甲状腺功能减退会降低内皮依赖性和一氧化氮依赖性血管扩张。由于甲状腺疾病引起的 HT 通常可以通过恢复甲状腺功能正常来逆转，但在某些情况下，需要进行药物治疗来控制血压。在甲状腺功能亢进中，β受体阻滞剂是控制血压的首选治疗方法，但当它们有禁忌证或不能耐受时，建议使用血管紧张素转换酶抑制剂或钙通道阻滞剂（CCB）。甲状腺功能减退是一种典型的低肾素 HT 形式，对 CCB 和利尿剂有更好的降压反应；事实上，在甲状腺功能减退中，低钠饮食似乎进一步改善了血压控制。需要进行随机临床试验来比较甲状腺疾病中降压治疗对血压控制的疗效。
