Blocking of the receptor-stimulated calcium entry into human platelets by verapamil and nicardipine.
Verapamil (ED50 = 3 x 10(-6) M) and nicardipine (ED50 = 10(-6) M) inhibited the platelet activating factor (PAF)-induced increase of free cytosolic calcium concentration [( Ca2+]i) in quin2-loaded human platelets. In a Ca-free medium containing 5 mM BaCl2, PAF stimulated the inflow of Ba2+ ions which is completely abolished by verapamil and nicardipine. Simultaneous determination of quin2 fluorescence and 45Ca absorption showed that the action of verapamil is accounted for by blocking of the Ca2+ entry. Nicardipine suppresses also Ca2+ mobilization from intracellular stores. The effects of verapamil and nicardipine are not competitive with respect to PAF. The blockers reduce the [Ca2+]i increase induced by ADP, vasopressin, and PGH2 analogue U46619.
Avdonin
P V
PV
Institute of Experimental Cardiology, USSR Cardiology Research Center, Moscow.
Men'shikov MYu
Svitina-Ulitina
I V
IV
Tkachuk
V A
VA
D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism; D006801:Humans; D009529:Nicardipine / Q000494:pharmacology*; D010972:Platelet Activating Factor / Q000494:pharmacology; D013050:Spectrometry, Fluorescence; D014700:Verapamil / Q000494:pharmacology*
D010972:Platelet Activating Factor; D014700:Verapamil; D009529:Nicardipine; D002118:Calcium