Amlodipine suppresses Ang-II-induced endothelium dysfunction by diminishing ROCK1 expression

Objective: To investigate the effects and mechanisms of amlodipine therapy on endothelium dysfunction induced by angiotensin-II (Ang-II) stimulation. Methods: Human umbilical vein endothelial cells (HUVECs) were used and divided into five groups: Blank control, Ang-II (10 −6  mol/L), levorotatory am...

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Published in:Clinical and experimental hypertension (1993) 2016-02, Vol.38 (2), p.166-172
Main Authors: Xu, Rulin, Cai, Anping, Zheng, Dongdan, Qiu, Ruofeng, Li, Liwen, Zhou, Yingling, Feng, Yingqing, Mai, Weiyi
Format: Article
Language:English
Subjects:
amlodipine
Amlodipine - pharmacology
Angiotensin II - pharmacology
Apoptosis - drug effects
bcl-2-Associated X Protein - drug effects
bcl-2-Associated X Protein - metabolism
Calcium Channel Blockers - pharmacology
endothelial function
Endothelium, Vascular - drug effects
Endothelium, Vascular - metabolism
Endothelium, Vascular - physiopathology
Human Umbilical Vein Endothelial Cells - drug effects
Human Umbilical Vein Endothelial Cells - metabolism
Humans
Hypertension - metabolism
Hypertension - physiopathology
Nitric Oxide - metabolism
Nitric Oxide Synthase Type III - drug effects
Nitric Oxide Synthase Type III - metabolism
Phosphoproteins - drug effects
Phosphoproteins - metabolism
Proto-Oncogene Proteins c-bcl-2 - drug effects
Proto-Oncogene Proteins c-bcl-2 - metabolism
Rho-associated kinase
rho-Associated Kinases - drug effects
rho-Associated Kinases - metabolism
Vasoconstrictor Agents - pharmacology
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Summary:Objective: To investigate the effects and mechanisms of amlodipine therapy on endothelium dysfunction induced by angiotensin-II (Ang-II) stimulation. Methods: Human umbilical vein endothelial cells (HUVECs) were used and divided into five groups: Blank control, Ang-II (10 −6  mol/L), levorotatory amlodipine (5 × 10 −6  mol/L) + Ang-II (10 −6  mol/L), dextrorotatory amlodipine (5 × 10 −6  mol/L) + Ang-II (10 −6  mol/L) and racemic amlodipine (5 × 10 −6  mol/L) + Ang-II (10 −6  mol/L) groups. Twenty-four hours later, HUVECs were collected for evaluating endothelial nitric oxide synthase (eNOS), p-eNOS, rho-associated kinase 1 (ROCK1), Bcl-2 and Bax expressions. Nitric oxide (NO) concentration within endothelium was also detected. Flow cytometry was conducted to assess HUVECs apoptosis. Results: With 24 hours of Ang-II stimulation, compared to blank control group, expressions of eNOS and p-eNOS and NO production were significantly reduced in Ang-II group (p 
ISSN:1064-1963
1525-6006
DOI:10.3109/10641963.2015.1081212