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Do lipophilic dihydropyridine calcium channel blockers inhibit ox-LDL induced proliferation and oxidative stress in vascular smooth muscle cells?
Do lipophilic dihydropyridine calcium channel blockers inhibit ox-LDL induced proliferation and oxidative stress in vascular smooth muscle cells?
Highly lipophilic calcium channel blockers like lacidipine inhibit ox-LDL-induced proliferation and oxidative stress in vascular smooth muscle cells, suggesting a potential mechanism for their vascular protective effects.
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Does not warrant changing CCB use in atherosclerosis; hypothesis-generating for lipophilic dihydropyridines' effects on VSMC proliferation.
BACKGROUND: Dihydropyridine calcium channel blockers (CCBs) are more effective in reducing carotid intima-media thickness (IMT) than other classes of antihypertensive drugs due to their vascular effects. However, the mechanism remains to be elucidated. FINDINGS: Ox-LDL induced HUVSMCs proliferation in a time- and dose-dependent manner. When pretreated with three CCBs before 50 μg/ml ox-LDL stimulation, 30 μM lacidipine and 3 μM amlodipine exhibited 27% and 18% decrease of pro-proliferative effect induced by ox-LDL, whereas (S-)-amlodipine did not have any anti-proliferative effect. 30 μM lacidipine inhibited about two-thirds of the ox-LDL induced ROS production in HUVSMCs, whereas amlodipine and (S-)-amlodipine did not have influence on ROS production. The MAPKs pathway inhibitors inhibited the ox-LDL induced proliferation of HUVSMCs. CONCLUSION: Our study has demonstrated that lipophilic CCBs, such as lacidipine may inhibit ox-LDL induced proliferation and oxidative stress of VSMCs, and that the ROS-MAPKs pathway might be involved in the mechanism.
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Zou et al. (2012) studied this question.
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