Endothelium-dependent vasodilation by rhTSH

TOPIC: Vascular effects of TSH

Title: Enhancement of vascular endothelial function by recombinant human thyrotrophin.

Authors: Napoli R, Biondi B, Guardasole V, D'Anna C, De Sena A, Pirozzi C, Terracciano D, Mazzarella C, Matarazzo M, & Sacca L.

Reference: Journal of Clinical Endocrinology & Metabolism 93: 1959-1963, 2008



The cardiovascular consequences of thyroid disease are attributed to the effects of thyroid hormones. There is limited information as to whether TSH affects the cardiovascular system.


To determine the effect of TSH on vascular homeostasis.


Two separate double-blind controlled studies were performed, one in 8 healthy volunteers and one in 6 thyroidectomised patients. Recombinant TSH (rhTSH) or saline was infused intra-brachially to raise TSH to about 100 μU/ml. Endothelium dependent and independent vasodilation was tested by intra-arterial infusion of acetylcholine and sodium nitroprusside, respectively, and measuring forearm blood flow by plethysmography.


rhTSH increased endothelium-dependent vasodilatation in control subjects and thyroidectomised patients to the same degree. There was no effect on endothelium independent vasodilation in either group. Serum T 3 increased during rhTSH infusion in the controls but not in thyroidectomised patients.


rhTSH exerts marked effects on vessel resistance by enhancing endothelium-mediated vasodilation, independent of changes in thyroid hormone concentrations.


It has not been clear whether TSH can affect vascular reactivity despite the knowledge that TSH receptors are found in endothelial cells and vascular smooth muscle cells of the cardiovascular system. Present study showed that, at least in the short term, TSH enhances vascular reactivity by increasing endothelium-mediated vasodilation independent of thyroid hormone concentration (because the same effects were observed in thyroidectomised patients who did not have any changes in serum T3).

From these data it seems that the increased risk of cardiovascular events associated with subclinical hypothyroidism is not due to the rise in circulating TSH concentrations. However, there is at least one other study suggesting a slight reduction in flow-mediated dilation in thyroidectomised patients. The role of the vascular smooth muscle cell in response to alterations in thyroid hormone also awaits clarification. This whole story will continue to flow.

Summary and commentary prepared by John Lazarus