Abnormal circulatory function in TRIC-A-knockout mice

本项目旨在探讨trica基因敲除小鼠高血压和异丙肾上腺素（Iso）诱导的肥厚等循环功能异常的致病机制。发现高血压是由敲除trica的血管平滑肌细胞的血管张力调节异常引起的。另一方面，在trica基因敲除小鼠中，渗透泵输注Iso可引起心肌纤维化，但不引起心肌肥大。不幸的是，在研究期间，心脏纤维化的机制尚不清楚。我们将试着在另一篇文章中研究这个项目。

The aim of this project is to examine the pathogenic mechanism of abnormal circulatory function such as hypertension and isoproterenol(Iso) induced hypertrophy in TRIC-A-knockout mice. It was found that hypertension was caused by abnormality of vascular tonus regulation in TRIC-A-knockout vascular smooth muscle cells. On the other hand, cardiac fibrosis but not hypertrophy was significantly induced by Iso infusion using osmotic pump in TRIC-A-knockout mice. Unfortunately, it was unclear the mechanism of cardiac fibrosis during research period. We will try to examine this project in another one.