Abstract
 
Vol 48 No. 4: 378-384 [PDF] [Full Text]
 
Atorvastatin blocks increased l-type Ca2+ current and cell injury elicited by angiotensin II via inhibiting oxide stress
 
Yanzhuo Ma1,†,*, Lingfeng Kong1,2,†,*, Shuying Qi1,* and Dongmei Wang1,*

1Department of Cardiology, Bethune International Peace Hospital, Shijiazhuang 050000, China
2Hebei Medical University, Shijiazhuang 050011, China
These authors contributed equally to this work.
 

Abstract  The l-type Ca2+ current (ICa,l) plays a crucial role in shaping action potential and is involved in cardiac arrhythmia. Statins have been demonstrated to contribute to anti-apoptotic and anti-arrhythmic effects in the heart. Here, we examined whether atorvastatin regulates the ICa,l and cell injury induced by angiotensin II (AngII) as well as the putative intracellular cascade responsible for the effects. Cultured neonatal rat ventricular myocytes were incubated with AngII for 24 h, and then cell injury and expression levels of Nox2/gp91phox, p47phox, and Cav1.2 were analyzed. In addition, ICa,l was recorded using the whole-cell patch-clamp technique, and mechanisms of atorvastatin actions were also investigated. It was found that the number of apoptotic cardiomyocytes was increased and cell viability was significantly decreased after AngII administration. AngII also augmented the expressions of Nox2/gp91phox and p47phox compared with control cardiomyocytes. Exposure to AngII evoked ICa,l in a voltage-dependent manner without affecting the ICV relationship. In addition, AngII enhanced membrane Cav1.2 expression. These effects were abolished in the presence of the reactive oxygen species (ROS) scavenger, manganese (III)-tetrakis 4-benzoic acid porphyrin [Mn(III)TBAP], or the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor, atorvastatin. These results suggested that atorvastatin mediates cardioprotection against arrhythmias and cell injury by controlling the AngIICROS cascade.

 

Keywords   atorvastatin; angiotensin II; l-type Ca2+ current; apoptosis

 

Received   2015-9-23  
Accepted  
2015-12-12

 

Funding  -

 

* Correspondence address  Tel/Fax: +86-311-87978302; E-mail: slwangdm@126.com

 
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