Why the study?
The study aimed to describe the functions of vascular endothelial cells in protecting target organs and the anti-atherosclerotic effects of different enantiomers of amlodipine in an atherosclerosis model.
Do different enantiomers of amlodipine improve lipid profiles and vasomotor factors in a rabbit model of atherosclerosis?
Do different enantiomers of amlodipine improve lipid profiles and vasomotor factors in a rabbit model of atherosclerosis?
In a rabbit model of atherosclerosis, amlodipine enantiomers protected endothelial function by reducing ET-1 and iNOS expression, without altering lipid profiles.
Amlodipine enantiomers may modulate endothelial markers independently of lipids in atherosclerotic rabbits; hypothesis-generating and leaves open human translation.
This research aimed to describe the functions of vascular endothelial cells (VECs) in protecting target organs and the anti-atherosclerotic effects of different enantiomers of amlodipine on a rabbit model of atherosclerosis. Thirty male New Zealand white rabbits were randomly allocated to four groups (nA = 9, nB = 7, nC = 7, and nD = 7 rabbits): rabbits in group-A (control group) were fed a high-fat diet, group-B rabbits were fed a high-fat diet plus 2.5 mg/kg/day S-amlodipine, group-C rabbits were fed a high-fat diet plus 2.5 mg/kg/day R-amlodipine, and group-D rabbits were fed a high-fat diet plus 5 mg/kg/day racemic amlodipine. Different enantiomers of amlodipine did not influence lipid profiles and serum level of eNOS in the rabbit atherosclerosis model but decreased ET-1 expression to some extent. The serum NO and iNOS levels in the drug intervention groups were significantly reduced. No significant differences in the rabbits' body weights were observed. At the 4th and 8th weeks, the serum lipid profiles significantly increased in high cholesterol diet groups. The serum ET-1 level was significantly increased in each group of rabbits at the 8th week. Both S-amlodipine and R-amlodipine may protect the endothelium by reducing the serum ET-1 level, downregulating iNOS expression.
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Zhang et al. (2021) studied this question.
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