Key result
The efficacy of calcium antagonists in suppressing experimental atherosclerosis remains controversial and may be due to nonspecific hemodynamic effects rather than specific calcium channel blockade.
Why the study?
Do calcium antagonists and other antihypertensive agents reduce experimental atherosclerosis in animal models?
Do calcium antagonists and other antihypertensive agents reduce experimental atherosclerosis in animal models?
The anti-atherogenic effects of calcium antagonists in experimental models remain controversial and may be driven by nonspecific hemodynamic effects shared by other antihypertensive agents.
Controversy on calcium antagonists for experimental atherosclerosis warrants caution against clinical extrapolation; leaves open specific vs hemodynamic mechanisms.
In 1981, Henry and Bentley first reported that nifedipine suppressed experimental atherosclerosis without inhibiting hypercholesterolemia in cholesterol-fed rabbits. Numerous studies have since been performed to determine whether calcium antagonists, a heterogenous group of compounds, possess significant anti-atherogenic activity; however, their efficacy in this respect remains controversial. Even if they are effective in controlling the development of atherosclerotic lesions, their observed effects in this respect may be unrelated to their effects on voltage-dependent Ca2+ channels. Rather, they may be due to nonspecific hemodynamic effects, in that other antihypertensive agents, such as reserpine, guanethidine, propranolol, metoprolol, and doxazosin, are also reported to be effective in controlling experimental atherosclerosis in normotensive and hypertensive animals. Comparative studies on calcium antagonists versus other antihypertensive agents are required to determine whether the benefit derived from the calcium antagonists in experimental atherosclerosis is specific for these antagonists.
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Naito et al. (1993) conducted a review in Experimental atherosclerosis. Calcium antagonists vs. Control was evaluated on Atherosclerosis development or regression. The efficacy of calcium antagonists in suppressing experimental atherosclerosis remains controversial and may be due to nonspecific hemodynamic effects rather than specific calcium channel blockade.
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