It is suggested that calcium antagonists can counteract the process of atherogenesis by influencing different cellular mechanisms, for example, inhibiting cellular migration and proliferation, as well as by having beneficial effects on lipid metabolism and platelet function. In an assessment of the activity of different calcium antagonists in various platelet function tests and prostacyclin (PGI2) synthesis, amlodipine, diltiazem, felodipine, isradipine, nicardipine, nifedipine, nitrendipine and verapamil were tested in vitro for their effects on adenosine diphosphate (ADP)- or collagen-induced platelet aggregation, malondialdehyde (MDA) formation and vascular PGI2 production. Nitrendipine, isradipine and nicardipine were shown to inhibit both ADP- and collagen-induced platelet aggregation at the lowest concentration (0.5 microgram/ml). The half-maximum inhibiting concentration (IC50) of isradipine (4.78 +/- 0.36 micrograms/ml for ADP-induced platelet aggregation) was significantly (p < 0.01) lower than the IC50 of all the other drugs. Nitrendipine, with an IC50 of 44.2 +/- 5.32 micrograms/ml, and nicardipine, with an IC50 of 46.74 +/- 3.83 micrograms/ml, were respectively the second and third most effective compounds. Formation of MDA was also inhibited the most by isradipine, which exerted its inhibitory properties at one-fifth the concentration needed with the other agents: the IC50 of isradipine was 0.98 +/- 0.16 microgram/ml, which was significantly different (p < 0.05) compared with the second most effective agent, verapamil, which had an IC50 of 14.92 +/- 3.78 micrograms/ml. In-vitro PGI2 production was stimulated the most by isradipine as well, producing a significant (p < 0.01) increase to 417.8 +/- 47.6 pg/mg tissue/h (control: 296.4 +/- 17.6 pg/mg tissue/h) at a concentration of 0.5 microgram/ml.(ABSTRACT TRUNCATED AT 250 WORDS)