Isradipine increases platelet--low-density lipoprotein binding: evidence from ex-vivo studies in humans.

The effects of isradipine (2.5 mg twice daily) on platelet--radioiodine-labeled [123I] low-density lipoprotein (LDL) binding were measured in 16 hypertensive patients (mean age 46.2 +/- 10.7 years) with (cholesterol > 250 mg/dl; n = 8) and without (cholesterol < 200 mg/dl; n = 8) hypercholesterolaemia during 4 weeks of isradipine treatment after 4 weeks of pretreatment placebo followed by 2 weeks of post-treatment placebo periods. Radioligand LDL-binding studies revealed that isradipine induced a significant (p < 0.001) rise in maximum binding capacity (Bmax) from a mean of 1148.6 +/- 244.3 ng protein/10(9) platelets to a mean of 1262.3 +/- 204.1 ng protein/10(9) platelets [dissociation constant (Kd): 9.7 +/- 4.9 micrograms protein/ml before treatment vs 7.8 +/- 3.7 g protein/ml after treatment]. After the post-treatment placebo phase, both Bmax and Kd returned to baseline levels. When the hypercholesterolaemic patients were compared with the normocholesterolaemics, the former revealed a more pronounced increase in platelet [125I]-LDL-binding capacity. Correspondingly, the dissociation constant showed a significantly (p < 0.05) greater decrease. In accordance with these results, both total and LDL cholesterol were reduced after 4 weeks of therapy with significant (p < 0.03) rises through to the end of the post-treatment placebo period. It is suggested that the observed increase in high-affinity platelet--LDL binding with isradipine treatment reflects a state of decreased in-vivo platelet activation, an effect which may be of particular clinical value in hyperlipidaemic patients.