TRPC1, CaN and NFATC3 signaling pathway in the pathogenesis and progression of left ventricular hypertrophy in spontaneously hypertensive rats

Abstract

Spontaneously hypertensive rats (SHR) was used to study left ventricular hypertrophy (LVH) and its dynamic change after the interventions with Telmisartan and Amlodipine. The results showed that the expression of TRPC1, CaN and NFATC3 increased gradually with the pathogenesis and progression of LVH. Telmisartan reduced blood pressure and LVH, and down-regulated the expression of TRPC1, CaN and NFATC3 in left ventricle of SHR. Amlodipine reduced the blood pressure in SHR but had no impact on the hypertrophy and expression of above factors. Our data suggest that the pathogenesis and progression of LVH in SHR are related to upregulation of TRPC1, CaN and NFATC3 signaling pathway.

• Amlodipine
• left ventricular hypertrophy
• spontaneously hypertensive rats
• Telmisartan
• TRPC1

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

The project was sponsored by National Natural Science Foundation (grant no. 81170143), Major Research Project Funds of Fujian Medical University (grant no. 09ZD010), National and Fujian Key Clinical Specialty Discipline Construction Programs.