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The antiatherosclerotic effect of the calcium antagonists and their implications in hypertension
W G Nayler1, S Panagiotopoulos
1Department of Medicine, University of Melbourne, Vic., Australia.
Insights
Manidipine, a long-acting calcium channel blocker (CCB), effectively reduces atherosclerotic lesion formation in animal models. This study demonstrates a dose-dependent effect without impacting plasma cholesterol levels, offering a potential new therapeutic avenue.
Area of Science:
- Cardiovascular Science
- Pharmacology
Background:
- Atherosclerotic lesion formation involves numerous calcium-dependent processes.
- Hypertension, a major risk factor, is linked to calcium's role in smooth muscle contraction.
- Previous studies demonstrated the efficacy of short-acting calcium channel blockers (CCBs) in preventing atherosclerosis.
Purpose of the Study:
- To investigate the effect of manidipine, a novel long-acting CCB, on atherosclerotic lesion formation.
- To determine if manidipine reduces lesion development independently of plasma cholesterol levels.
Main Methods:
- An animal model was used to study the effects of manidipine.
- Dose-dependent administration of manidipine was employed.
- Plasma cholesterol levels were monitored.
Main Results:
- Manidipine demonstrated a dose-dependent reduction in atherosclerotic lesion formation.
- The observed reduction in lesion formation was not associated with changes in plasma cholesterol.
- This suggests a direct anti-atherosclerotic effect of manidipine.
Conclusions:
- Long-acting manidipine effectively inhibits atherosclerotic lesion development in this animal model.
- Manidipine offers a potential therapeutic strategy for atherosclerosis, acting independently of lipid-lowering effects.
- Further clinical investigation is warranted to confirm these findings in humans.
Abstract:
Calcium-dependent processes involved in atherosclerotic lesion formation include platelet aggregation, monocyte adhesion, release of growth factors, cell proliferation and migration, protein and collagen secretion and synthesis, and endothelial necrosis. In addition, the calcium (Ca2+) component of smooth muscle cell contraction contributes to one of the main risk factors, hypertension. The ability of the calcium channel blockers (CCBs) to interrupt the sequence of events that culminates in the formation of atherosclerotic lesions has been demonstrated in animal models and clinical trials. These studies have involved the short-acting CCBs. The results of this animal study show that manidipine, a new long-acting CCB, produces a dose-dependent reduction in atherosclerotic lesion formation without reducing plasma cholesterol.
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