维拉帕米和硝苯地平对受体刺激的钙进入人血小板的阻断作用。

Blocking of the receptor-stimulated calcium entry into human platelets by verapamil and nicardipine.

作者信息

Avdonin P V, Svitina-Ulitina I V, Tkachuk V A

机构信息

Institute of Experimental Cardiology, USSR Cardiology Research Center, Moscow.

出版信息

Thromb Res. 1988 Dec 15;52(6):587-97. doi: 10.1016/0049-3848(88)90131-4.

DOI:10.1016/0049-3848(88)90131-4

PMID:3232128

Abstract

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.

摘要

维拉帕米（半数有效剂量=3×10⁻⁶M）和尼卡地平（半数有效剂量=10⁻⁶M）抑制血小板活化因子（PAF）诱导的用喹啉-2负载的人血小板中游离细胞溶质钙浓度[Ca²⁺]i的升高。在含有5mM BaCl₂的无钙培养基中，PAF刺激Ba²⁺离子内流，这被维拉帕米和尼卡地平完全消除。同时测定喹啉-2荧光和⁴⁵Ca摄取表明，维拉帕米的作用是通过阻断Ca²⁺内流来实现的。尼卡地平也抑制Ca²⁺从细胞内储存库的动员。维拉帕米和尼卡地平的作用相对于PAF而言并非竞争性的。这些阻滞剂降低了由ADP、血管加压素和PGH₂类似物U46619诱导的[Ca²⁺]i升高。