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Protective effects of diltiazem against vascular endothelial cell injury induced by angiotensin‐ II and hypoxia
Author(s) -
Li Minggao,
Li Jing,
Meng Guo,
Liu Xin
Publication year - 2015
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12371
Subject(s) - diltiazem , hypoxia (environmental) , calcium in biology , pharmacology , angiotensin ii , endothelial stem cell , calcium , intracellular , chemistry , apoptosis , mitochondrion , medicine , endocrinology , in vitro , biochemistry , receptor , oxygen , organic chemistry
Summary To provide pharmacological data for future clinical studies, this study investigated the protective effects of diltiazem on vascular endothelial cell ( VEC ) injury induced by angiotensin‐ II (Ang II ), hypoxia, and a combination of both treatments. The concentration of intracellular free calcium and the mitochondrial membrane potential in VEC were assessed as indicators of cell injury. An in vivo hypoxic animal model was used to test the protective effect of diltiazem on vascular endothelial tissues. Our study showed that Ang II and hypoxia decreased the mitochondrial membrane potential in VEC , which was significantly inhibited by diltiazem. Diltiazem protected against VEC injury induced by the increased concentration of intracellular free calcium, which was associated with Ang II and hypoxia. Diltiazem reduced the apoptosis of rat VEC under a sustained hypoxic condition. In addition, it reduced Ang II and endothelin I levels in rat vascular endothelial tissues. Our study confirmed that Ang II and hypoxia induced VEC injury by regulating the levels of mitochondrial membrane potential and intracellular free calcium. Diltiazem, a calcium channel blocker, protected VEC from Ang II ‐ and hypoxia‐induced injury.