Protective effects of diltiazem against vascular endothelial cell injury induced by angiotensin‐II and hypoxia. (April 2015)

• Record Type: Journal Article
• Authors: Li, Minggao; Li, Jing; Meng, Guo; Liu, Xin
• Is Part Of: Clinical and experimental pharmacology and physiology. Volume 42:Number 4(2015:Apr.)
• Page Start: 337
• Page End: 343
• Publication Date: 2015-04
• Subjects: angiotensin‐II (AngII) -- diltiazem -- hypoxia -- vascular endothelial cells; Clinical pharmacology -- Periodicals; Pharmacology, Experimental -- Periodicals; Physiology, Experimental -- Periodicals; Physiology, Pathological -- Periodicals; 615.1
• DOI: 10.1111/1440-1681.12371
• Languages: English
• ISSNs: 0305-1870

Abstract

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 (AngII), 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 AngII 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 AngII and hypoxia. Diltiazem reduced the apoptosis of rat VEC under a sustained hypoxic condition. In addition, it reduced AngII and endothelin I levels in rat vascular endothelial tissues. Our study confirmed that AngII 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 AngII‐ and hypoxia‐induced injury.