Men'shikov M Iu, Avdonin P V, Negresku E V, Bugriĭ E M, Svitina-Ulitina I V
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR. 1986;9(2):25-30.
The effect of calcium antagonists (verapamil, nicardipine, nifedipine), nitrates (glycerin trinitrate, isosorbide dinitrate and sodium nitroprusside) and of antiarrhythmic drugs (ethmozin, ethacizin) on the increase of platelet Ca2+ concentration brought about by aggregation inductors was studied. All the analyzed substances produced an inhibitory effect on the induction of cellular Ca2+ level increase due to the action of platelet aggregation factor, ADP, vasopressin and endoperoxide PGH2 stable analogue. The degree of this inhibitory effect of calcium antagonists and nitrates was independent of the nature of the stimulator used. Calcium-blocking action of calcium antagonists and nitrates was due to suppression of the entry of Ca2+ into the cells. The action of nitrates on platelets was accompanied by an acceleration of cGMP and cAMP synthesis. Unlike nitrates, antiarrhythmic drugs did not influence the intracellular level of cyclic nucleotides. On the basis of the data obtained it is suggested that calcium-blocking action of different types of compounds can be mediated by different intracellular mechanisms.
研究了钙拮抗剂(维拉帕米、尼卡地平、硝苯地平)、硝酸盐类(硝酸甘油、异山梨醇二硝酸酯和硝普钠)以及抗心律失常药物(乙莫嗪、乙卡嗪)对聚集诱导剂引起的血小板Ca2+浓度升高的影响。所有被分析的物质对因血小板聚集因子、ADP、血管加压素和内过氧化物PGH2稳定类似物的作用而导致的细胞Ca2+水平升高的诱导均产生抑制作用。钙拮抗剂和硝酸盐类这种抑制作用的程度与所用刺激剂的性质无关。钙拮抗剂和硝酸盐类的钙阻断作用是由于抑制了Ca2+进入细胞。硝酸盐类对血小板的作用伴随着cGMP和cAMP合成的加速。与硝酸盐类不同,抗心律失常药物不影响细胞内环核苷酸的水平。根据所获得的数据表明,不同类型化合物的钙阻断作用可能由不同的细胞内机制介导。