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Isolation and Characterization of Primary Rat Valve Interstitial Cells: A New Model to Study Aortic Valve Calcification
Published on: November 20, 2017
Aortic cell apoptosis in rat primary aldosteronism model.
Yongji Yan1, Jinzhi Ouyang, Chao Wang
1Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. 7577yyj@163.com
Summary
Aldosterone directly causes vascular cell apoptosis in the aorta through mineralocorticoid receptors, independent of blood pressure. This process involves the Bcl-2/Bax pathway and contributes to vascular injury.
Area of Science:
- Cardiovascular Biology
- Endocrinology
- Molecular Biology
Background:
- Aldosterone is a key hormone in regulating blood pressure and electrolyte balance.
- Its role in direct vascular cell apoptosis and injury is not fully understood.
Purpose of the Study:
- To investigate if aldosterone induces vascular cell apoptosis in vivo.
- To elucidate the molecular mechanisms and receptor pathways involved.
Main Methods:
- Rats were infused with aldosterone, with or without eplerenone or hydralazine.
- Systolic blood pressure, plasma aldosterone concentration, and renin activity were measured.
- Aortic apoptosis, cytochrome c, caspase-3, Bax, and Bcl-2 levels were assessed.
Main Results:
- Aldosterone increased blood pressure, plasma aldosterone concentration, and aortic apoptosis.
- Elevated levels of cytochrome c, activated caspase-3, and altered Bax/Bcl-2 ratios were observed.
- Eplerenone, but not hydralazine, inhibited these aldosterone-induced effects.
Conclusions:
- Aldosterone directly induces vascular cell apoptosis in the aorta via mineralocorticoid receptors.
- This effect is independent of blood pressure elevation.
- Aldosterone-mediated vascular apoptosis may contribute to vascular injury.
