INFLUENCE OF MIBEFRADIL ON CA2+ INFLUX INDUCED BY VASOACTIVE HORMONESOR DEPLETION OF INTRACELLULAR CALCIUM STORES

The influence of the new calcium antagonist mibefradil (GAS 116666-63- 8, Ro 405967) on calcium influx into rabbit smooth muscle cells (VSMC) was studied. Angiotensin II-stimulated divalent cations entry was blo cked by mibefradil at micromolar concentrations (1-10 mu mol/l). In th e same range of concentrations, the antagonist depressed capacitative calcium influx evoked by thapsigargin- and 2,5-di-tert-butylhydroquino ne (BHQ)-dependent depletion of internal depots. The ability to block the receptor-mediated pathway of calcium current into VSMC may explain in part the difference between the mode of pharmacological action of mibefradil as compared to other calcium antagonists.