Not much has been reported about the effects of
hyperthyroidism and its correction on resistance vessels, and just two inconsistent studies have investigated the impacts of restored euthyroidism on vascular reactivity. In this regard, we designed the current study to evaluate the vascular reactivity of the mesenteric arteries of
hyperthyroid and restore euthyroid rats.
Hyperthyroidism was induced by administration of
triiodothyronine (T3; 300μg/kg, i.p., for 12 weeks in T3 group). Euthyroidism was restored by administration of T3 for 8 weeks and then T3+Methimazole (0.003% in
drinking water) for 4 weeks (T3+MMI group). According to the McGregor method, vascular relaxation and contractility response were measured in response to
acetylcholine or
phenylephrine respectively. We found that maximal contractility response (Emax) to
phenylephrine in the T3 group was significantly decreased (P<0.001), and Emax to
acetylcholine was significantly increased compared with the saline group (P<0.05). When
N(G)-nitro-L-arginine methyl ester (L-NAME, 3×10(-4)M) was used, Emax to
acetylcholine in the T3 group was still higher than the saline group (P<0.05). However, decrease in maximal response of the T3 group was significantly greater than the saline group (P<0.01). We also showed that when euthyroidism is restored by
methimazole therapy, enhanced
acetylcholine-induced vasorelaxation and impaired contractility response to
phenylephrine were normalized, as there was no significant difference in Emax of the T3+MMI group versus the saline group (P>0.05). In conclusion, synthesis of both
nitric oxide (NO) and endothelium-derived hyperpolarizing factor (
EDHF) in mesenteric arteries significantly increased as a consequence of
hyperthyroidism, and this abnormal vascular reactivity is corrected by
methimazole therapy.