[Calcium antagonists nicardipine and verapamil suppress Ca(2+) entry and activate Na(+) entry into platelets].
In micromolar concentrations both antagonists suppressed CA2+ entry and simultaneously elevate the agonist-induced plasma membrane depolarization due to Na+ inward current via these channels. Potentiation by nicardipine of the Na+ current induced by the platelet-activating factor, was revealed. Both antagonists caused plasma membrane depolarization suppressed by Na+ and Ca2+ ions. The depolarization disappeared after substitution of NaCl by an isotonic solution of choline chloride. The antagonists nicardipine and verapamil seem to modulate the platelet receptor-operated channels suppressing Ca2+ entry and elevating Na+ current via these channels.
Cheglakov
I B
IB
Koltzov Institute of Developmental Biology, Russian Acad. Sci., Russia.
Avdonin
P V
PV
D001572:Benzofurans; D052160:Benzothiazoles; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002232:Carbocyanines; D004988:Ethers, Cyclic; D005456:Fluorescent Dyes; D006801:Humans; D066298:In Vitro Techniques; D009529:Nicardipine / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000502:physiology; D014700:Verapamil / Q000494:pharmacology*
D001572:Benzofurans; D052160:Benzothiazoles; D002121:Calcium Channel Blockers; D002232:Carbocyanines; D004988:Ethers, Cyclic; D005456:Fluorescent Dyes; D015222:Sodium Channels; C061665:sodium-binding benzofuran isophthalate; C012944:3,3'-dipropyl-2,2'-thiadicarbocyanine; D012964:Sodium; D014700:Verapamil; D009529:Nicardipine; D002118:Calcium