Abstract
Low thyroid hormone (TH) function has been linked to impaired coronary blood flow, reduced density of small arterioles, and heart failure. Nonetheless, little is known about the mechanisms by which THs regulate coronary microvascular remodeling. The current study examined the initial cellular events associated with coronary remodeling induced by triiodothyronine (T3) in hypothyroid rats. Rats with established hypothyroidism, eight weeks after surgical thyroidectomy (TX), were treated with T3 for 36 or 72 hours. The early effects of T3 treatment on coronary microvasculature were examined morphometrically. Gene expression changes in the heart were assessed by quantitative PCR Array. Hypothyroidism resulted in arteriolar atrophy in the left ventricle. T3 treatment rapidly induced small arteriolar muscularization and, within 72 hours, restored arteriolar density to control levels. Total length of the capillary network was not affected by TX or T3 treatment. T3 treatment resulted in the coordinate regulation of Angiopoietin 1 and 2 expression. The response of Angiopoietins was consistent with vessel enlargement. In addition to the well known effects of THs on vasoreactivity, these results suggest that THs may affect function of small resistance arteries by phenotypic remodeling of vascular smooth muscle cells (VSMC).
Highlights
thyroid hormone (TH) affect diastolic and systolic function and peripheral vascular tone [1]
Do heart failure patients have a higher incidence of low TH function, the HUNT study showed that higher levels of thyroid stimulating hormone (TSH), which are still within the normal range, are associated with increased coronary artery disease mortality in women and unfavorable serum lipids in all patients [3,4]
One group of TX rats was treated for 36 hours and another group was treated for 72 hours
Summary
Chronic hypothyroidism can lead to severe left ventricular dysfunction, chamber dilatation, impaired coronary blood flow, reduced density of small arterioles, and eventual heart failure [2]. Animal studies demonstrated beneficial effects of THs on cardiac remodeling and function in dilated cardiomyopathy, hypertension, and myocardial infarction without increasing heart rate above normal values [6,7,8,9]. Of particular relevance to the current study, we demonstrated impaired resting and maximum blood flow in BIO-TO2 hamsters, subclinical hypothyroidism, and normalization of blood flow after TH treatment, which led to dramatic benefits on underlying cardiac pathology [6]. The above reports suggest that more information is needed regarding TH regulation of small resistance vessels in the heart since they may play an important role in coronary blood flow in heart diseases, in borderline low TH conditions
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