Impact of hyperthyroidism and its correction on vascular reactivity in humans .

BACKGROUND: Although thyroid hormone (TH) exerts relevant effects on the cardiovascular system, it is unknown whether TH also regulates vascular reactivity in humans. Methods and Results- We studied 8 patients with hyperthyroidism, basally (H) and 6 months after euthyroidism was restored by methimazole (EU). Thirteen healthy subjects served as control subjects (C). We measured forearm blood flow (FBF) by strain-gauge plethysmography during intrabrachial graded infusion of acetylcholine, sodium nitroprusside (SNP), norepinephrine, and L-NMMA (inhibitor of NO synthesis). Basal FBF (in mL. dL(-1). min(-1)) was markedly higher in H than in C (5.8+/-1.2 and 1.9+/-0.1, respectively; P<0.001) and was close to normal in EU (2.6+/-0.3, P<0.01 versus H). During acetylcholine infusion, FBF increased much more in H (+33+/-5) than in C (+14+/-3, P<0.01 versus H) and in EU (+20+/-5, P=0.01 versus H and P=NS versus C). In contrast, the response to SNP infusion was comparable in the patients and control subjects. During norepinephrine infusion, the fall in FBF was much more pronounced in H (-6+/-1) than in C (-0.7+/-0.3, P<0.005 versus H) and in EU (-1.5+/-0.3, P<0.01 versus H). Finally, inhibition of NO synthesis by L-NMMA decreased FBF by 2.8+/-0.6, 0.61+/-0.7, and 1.4+/-0.3 in H, C, and EU, respectively (H versus C and EU, P<0.05). CONCLUSIONS: In hyperthyroidism, (1) the marked basal vasodilation is largely accounted for by excessive endothelial NO production, (2) vascular reactivity is exaggerated because of enhanced sensitivity of the endothelial component, (3) the vasoconstrictory response to norepinephrine is potentiated, and (4) this abnormal vascular profile is corrected when euthyroidism is restored by medical therapy. The data demonstrate that vascular endothelium is a specific target of T