[Calcium antagonists: anti-atherosclerotic effect by modification of the prostaglandin system].

The aim of the study was to investigate the influence of calcium blockers on the prostaglandin system of blood platelets and the vessel wall with respect to a possible beneficial effect on atherosclerosis. The influence of diltiazem, isradipine, nifedipine and verapamil was examined on ADP- and collagen-induced in vitro platelet aggregation, platelet malondialdehyde formation and other platelet function tests. All the calcium blockers investigated inhibited platelet activation in a dose-dependent manner, isradipine being the most effective. Malondialdehyde formation (measured photometrically) and thromboxane (TX) B2 production were decreased too. Vascular tissue PG12 formation was investigated in rat aortic rings (6-oxo-PGF1 alpha-RIA). PG12 formation was enhanced by all the calcium blockers investigated (p less than 0.01), isradipine again having the most pronounced effect. Platelet adenylate cyclase was stimulated by diltiazem only (RIA, HPLC). Ex vivo ADP-, collagen- and epinephrine-induced platelet aggregation and serum TX were studied 90 minutes after ingestion to diltiazem (60 mg), nifedipine (20 mg) and verapamil (40 mg). ADP- and epinephrine-induced platelet aggregation (19-36%) and serum TX were reduced significantly (p less than 0.01), but collagen-induced aggregation was not significantly affected. These results suggest a possibly beneficial effect of calcium blockers on atherosclerosis via the prostaglandin system.