Context: The cardiovascular consequences of thyroid diseases are attributed to the altered secretion of thyroid hormones. The possibility that also thyrotropin (TSH) affects the cardiovascular system has been poorly explored. Endothelial cells and vascular smooth muscle cells possess TSH receptors.

Objective: The study was designed to determine whether TSH exerts any effect on vascular homeostasis.

Subjects and Methods: Two different double-blind, controlled studies were performed, one in eight healthy volunteers and the other in six thyroidectomized patients. rhTSH (or saline) was infused intra-brachially (1 mU/min) to raise TSH to severe hypothyroidism levels (100 µU/ml). Endothelium-dependent and –independent vasodilation was tested by intra-arterial infusion of acetylcholine (Ach) and sodium nitroprusside (NP), respectively, and forearm blood flow (FBF) was measured by plethysmography.

Results: Endothelium-dependent vasodilation was potentiated by rhTSH (p<0.05 for the treatment effect; General Linear Model). The dynamics of the response was also profoundly affected by rhTSH because the dose-response curve was much steeper than in controls (p<0.02 for the interaction between TSH and Ach). rhTSH had no effect on endothelium-independent vasodilation (P=NS for both treatment and interaction). During rhTSH infusion, free T3 levels increased slowly from 2.3±0.2 to 3.6±0.2 pg/ml. In thyroidectomized patients, rhTSH potentiated endothelium-mediated vasodilation to a similar extent than in healthy subjects (p=0.05 for the treatment effect and p=0.01 for the interaction), without affecting the response to NP. In these patients, thyroid hormones remained unchanged during rhTSH infusion.

Conclusions: rhTSH exerts marked effects on the resistance vessels by enhancing endothelial-mediated vasodilation, independent of changes in thyroid hormone concentration.