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Hypothyroidism has been recognized as a cause of secondary hypertension [1,2]. The most common type of hypothyroidism is that caused by primary thyroid gland failure. Basic causes of primary hypothyroidism are autoimmune, silent, postablative, goitrous, athyreotic and nonautoimmune (e.g., Riedel's), and subacute thyroiditis [3]. Chronic autoimmune lymphocytic thyroiditis (Hashimoto's disease) is the most common cause of thyroid gland dysfunction. Replacement of lacking thyroid hormones reduces high blood pressure (BP) and total cardiovascular risk [4]. Similar effects have also been described in subclinical hypothyroidism [5].
Systolic or diastolic hypertension?
Previous studies on the prevalence of hypertension in subjects with hypothyroidism have demonstrated elevated systolic or diastolic BP values, whereas one study has reported no association between hypertension and hypothyroidism (Table 1) [2,6-13]. Saito et al. found that diastolic BP correlated significantly with thyroxine (T4) and 3,5,3´-triiodothyronine (T3) in slightly hypothyroid females over 50 years of age [2].
Mechanisms of hypothyroidism-related hypertension
Increase in peripheral vascular resistance
To exert its cellular activity, T4 is converted to T3 via the enzymatic action of iodothyronine deiodinase. The two types of iodothyronine deiodinase, type I (DI) and II (DII), are expressed in different tissues. DI has been found in the thyroid gland, liver, kidneys and other tissues and DII in a limited number of tissues, such as the CNS, anterior pituitary tissue, human skeletal muscle and brown fat in the rat [14,15]. DI activity is known to be decreased in the hypothyroid state and may play a primary role in regulating circulating T3 levels, while DII activity is increased in hypothyroidism and probably regulates intracellular T3 concentrations.
3,5,3´-triiodothyronine represents the metabolically active thyroid agent that possibly has a vasodilatory effect on the vascular muscle cells [16]. Hypothyroidism and T3 deficiency are associated with peripheral vasoconstriction [17]. DII was identified in cultured human coronary and aortic arterial smooth muscle cells. DII is believed to be responsible for the local conversion of T4 to T3 in these vessels. It has been demonstrated that the expression of DII in vascular smooth muscle cells is dependent on a cAMP-mediated mechanism [18]. T3 inhibits DII activity at the pretranslational level (inhibition of DII mRNA expression). DII expression has been reported to be increased in hypothyroidism and to have a protective action on human vessels....