Yoneda K, Takasu N, Higa S, Oshiro C, Oshiro Y, Shimabukuro M, Asahi T
Second Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, Okinawa, Japan.
Thyroid. 1998 Jul;8(7):609-13. doi: 10.1089/thy.1998.8.609.
To determine whether thyroid hormones, triiodothyronine (T3) and thyroxine (T4), have any direct, nongenomic effects on vascular smooth muscle cells, we evaluated the effects of these hormones on rat coronary arteries. Bolus injection of T3 or T4 elicited a transient, dose-dependent decrease in coronary perfusion pressure (CPP), as well as an increase in arterial vasodilation. Vasodilation occurred immediately after injection, peaked at 15 seconds, and lasted 80 seconds. Reverse T3 had no effect on CPP or vasodilation. The rapidity of these effects suggests that they are not mediated by the T3-nuclear receptor, but are direct, nongenomic effects of thyroid hormones. Our results also suggest that thyroid hormones may play a role in preventing myocardial ischemia by inducing coronary artery vasodilation.
为了确定甲状腺激素三碘甲状腺原氨酸（T3）和甲状腺素（T4）是否对血管平滑肌细胞有任何直接的非基因组效应，我们评估了这些激素对大鼠冠状动脉的影响。推注T3或T4会引起冠状动脉灌注压（CPP）短暂的、剂量依赖性降低，以及动脉血管舒张增加。注射后立即出现血管舒张，在15秒时达到峰值，并持续80秒。反式T3对CPP或血管舒张没有影响。这些效应的快速性表明它们不是由T3核受体介导的，而是甲状腺激素的直接非基因组效应。我们的结果还表明，甲状腺激素可能通过诱导冠状动脉血管舒张在预防心肌缺血中发挥作用。
