Hyperthyroidism is due to exaggerated thyroid hormone bioactivity. We reviewed the vasculopathy in hyperthyroid rats through the following ways: 1) the voltage-gated calcium channels in vascular smooth muscle (VSM); 2) the receptor-operated calcium channels in VSM; 3) the different responses to catecholamines in VSM; 4) endothelium dependent/ independent relaxation; 5) the KATP channels; and 6) the altered allergic vascular responses. In the hyperthyroid state, the elevated intracellular calcium release and the impaired nitric oxide bioavailability resulted in abnormalities in vascular activities, which may be secondary to oxidative stress. The compromised vascular function consequent on the endothelial impairment observed in hyperthyroidism was also found in other diseases, such as neuro-degenerative disorders and diabetes. The study on these vascular alterations may throw a light on the understanding of mechanisms underlying vascular diseases.
Keywords: hyperthyroidism, vascular smooth muscle, nitric oxide, calcium channels, oxidative stress, allergy, endothelium, diabetes
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