The nonhemodynamic actions of nifedipine and some other calcium antagonists are, reviewed with regard to their relevance to the vasculoprotective and antiarteriosclerotic action of calcium antagonists. Nifedipine, and in order of declining potency, verapamil and diltiazem were shown to inhibit vascular myocyte proliferation and migration. Also, the incorporation of cholesteryl esters into macrophages or myocytes was inhibited by dihydropyridines and verapamil but not be diltiazem. The cholesterol and calcium contents were found to be lowered in the aortae of hypercholesterinemic rabbits treated chronically with dihydropyridine calcium antagonists. Replacement of damaged vascular endothelium and internal elastic lamina was seen in hypertensive Dahl-S rats after 6 weeks of antihypertensive treatment with nifedipine.
In addition to their blood-pressure lowering action, these nonhemodynamic effects might be involved in the prevention and reversal of hypertensive vascular disease and neuropathologic symptoms observed after the treatment of hypertensive rats with nifedipine or other dihydropyridine calcium antagonists since these therapeutic effects were also seen after blood-pressure neutral doses.
Key words nitrendipine - nimodipine - diltiazem - verapamil - myocyte proliferation - chronic treatment - experimental hypertension - calcium antagonist - parathyroid hormone - myocte migration