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Updated: Jul 29, 2026
Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
Published on: June 29, 2014
The protective effect of isosteviol sodium on cardiac function and myocardial remodelling in transverse aortic
Qingjin Ke1, Fei Liu1, Yuxin Tang1
1Institute of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Insights
Isosteviol sodium (STVNa) effectively reverses pressure overload-induced cardiac hypertrophy and fibrosis in rats. This compound shows promise for treating heart failure, even improving autonomic nervous system function.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Pathological cardiac hypertrophy is a major contributor to heart failure with limited effective treatments.
- Isosteviol has demonstrated cardioprotective effects against ischemia-reperfusion injury and isoproterenol-induced hypertrophy, but its efficacy in pressure overload models was unknown.
Purpose of the Study:
- To investigate the therapeutic effects of isosteviol sodium (STVNa) on pressure overload-induced cardiac hypertrophy.
- To evaluate STVNa's impact on cardiac function, fibrosis, and autonomic nervous system activity in a rat model.
Main Methods:
- A rat model of cardiac hypertrophy was induced using transverse aortic constriction (TAC).
- Cardiac function, electrocardiograms, and histological analyses were performed.
- In vitro studies assessed STVNa's effects on adult rat ventricular cell calcium transients and neonatal rat cardiac fibroblast proliferation.
Main Results:
- TAC induced significant cardiac hypertrophy, dysfunction, and electronic remodeling by 9 weeks.
- STVNa treatment reversed these TAC-induced changes, showing superiority over sildenafil in some aspects and without significantly altering calcium transients.
- STVNa also ameliorated cardiac fibrosis and inhibited TGF-β1-induced fibroblast proliferation, while uniquely improving autonomic nervous system function.
Conclusions:
- Isosteviol sodium is a potent therapeutic agent for pressure overload-induced cardiac hypertrophy and associated pathologies.
- STVNa offers a promising therapeutic strategy for heart failure, potentially by addressing fibrosis and autonomic dysfunction.
Abstract:
Pathological hypertrophy contributes to heart failure and there is not quite effective treatment to invert this process. Isosteviol has been shown to protect the heart against ischaemia-reperfusion injury and isoproterenol-induced cardiac hypertrophy, but its effect on pressure overload-induced cardiac hypertrophy is still unknown. Pressure overload induced by transverse aortic constriction (TAC) causes cardiac hypertrophy in rats to mimic the pathological condition in human. This study examined the effects of isosteviol sodium (STVNa) on cardiac hypertrophy by the TAC model and cellular assays in vitro. Cardiac function test, electrocardiogram analysis and histological analysis were conducted. The effects of STVNa on calcium transient of the adult rat ventricular cells and the proliferation of neonatal rat cardiac fibroblasts were also studied in vitro. Cardiac hypertrophy was observed after 3-week TAC while the extensive cardiac dysfunction and electronic remodelling were observed after 9-week TAC. Both STVNa and sildenafil (positive drug) treatment reversed the two process, but STVNa appeared to be more superior in some aspects and did not change calcium transient considerably. STVNa also reversed TAC-induced cardiac fibrosis in vivo and TGF-β1-induced fibroblast proliferation in vitro. Moreover, STVNa, but not sildenafil, reversed impairment of the autonomic nervous system induced by 9-week TAC.
