Hyperthyroidism enhances endothelium‐independent relaxation in rat aorta.

Abstract

Thyroid hormone (T3) is known to promote vascular relaxation. However, the molecular mechanisms of T3 actions are incompletely characterized. Considering our previous study where T3 rapidly stimulated nitric oxide (NO) production by vascular smooth muscle cell (VSMC), we hypothesized that NO derived from smooth muscle represents an important component to mediate the vasodilators effects of T3. In vitro, chronic treatment of VSMCs for 24h with T3 stimulated NO production, and decreased expression of contractile proteins alpha actin, calponin as well as MLC phosphorylation levels. In vivo, aortas isolated from rats submitted to experimental hyperthyroidism (7ug/100g T3 for 14 days) presented decreased on expression of contractile apparatus proteins, as well as alterations in vascular reactivity. Functional assays demonstrated that relaxation responses to sodium nitroprusside (SNP) were greater in endothelium‐denuded aortic rings from T3‐treated rats and phenylephrine‐induced contraction was reduced. These results suggest that enhanced NO‐mediated vasodilation as well as decreased responses to constrictor stimuli contribute to vascular relaxation during hyperthyroidism. Financial support: NIH (USA), FAPESP (Brazil).