Aortic cell apoptosis in rat primary aldosteronism model
Autor: | Zhun Wu, Dao-jing Gong, Xu Zhang, Xin Ma, Zheng Hu, Hua Xu, Jinzhi Ouyang, Baojun Wang, Yong-ji Yan, Jun Li, Chao Wang, Hongzhao Li, Taoping Shi, Dong Ni |
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Rok vydání: | 2010 |
Předmět: |
Male
medicine.medical_specialty medicine.drug_class Biomedical Engineering Apoptosis Biology Biochemistry Plasma renin activity Rats Sprague-Dawley Biomaterials Random Allocation chemistry.chemical_compound Primary aldosteronism Mineralocorticoid receptor Internal medicine Hyperaldosteronism Genetics medicine Animals Aldosterone Aorta Earth-Surface Processes Endothelial Cells Hydralazine medicine.disease Rats Eplerenone Receptors Mineralocorticoid Endocrinology chemistry Mineralocorticoid medicine.drug |
Zdroj: | Journal of Huazhong University of Science and Technology [Medical Sciences]. 30:385-390 |
ISSN: | 1993-1352 1672-0733 |
DOI: | 10.1007/s11596-010-0362-3 |
Popis: | This study aimed to determine whether aldosterone could induce vascular cell apoptosis in vivo. Thirty-two male rats were randomly divided into 4 groups: vehicle (control), aldosterone, aldosterone plus eplerenone or hydralazine. They were then implanted with an osmotic mini-pump that infused either aldosterone or the vehicle. Systolic blood pressure (SBP) was measured weekly by the tail-cuff method. After 8 weeks, plasma aldosterone concentration (PAC) and renin activity (PRA) were determined by radioimmunoassay. Aortic apoptosis was examined by TUNEL assay. The levels of cytochrome c and caspase-3 were determined by Western blotting and the expression of Bax and Bcl-2 was detected by immunohistochemistry and Western blotting. The results showed that as compared with control group, aldosterone-infused rats exhibited: (1) an increase in SBP; (2) significantly elevated PAC with depressed PRA; (3) elevated aortic vascular cell apoptosis accompanied with higher levels of cytochrome c and activated caspase-3; and (4) significantly up-regulated Bax protein with down-regulated Bcl-2. These effects of aldosterone were significantly inhibited after co-administration with eplerenone but not with hydralazine. It was concluded that aldosterone induced vascular cell apoptosis by its direct effect on the aorta via mineralocorticoid receptors and independently of blood pressure, which may contribute to aldosterone-mediated vascular injury. |
Databáze: | OpenAIRE |
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