Abstract
The search for compounds that selectively suppress the activity of plasma membrane Ca 2+ channels in electrically nonexcitable cells is a topical medicobiological problem. This was the first study to demonstrate that the antianginal drug trimetazidine selectively suppressed the activity of Ca 2+ channels activated by a drop in the Ca 2+ level in intracellular calcium stores in HL-60 human promyelocytes, the precursors of blood neutrophils and monocytes. It is principally important that trimetazidine as such did not induce Ca 2+ release from inositol triphosphate-sensitive Ca 2+ stores and did not activate Ca 2+ channels regulated by these stores. The results of this study allowed us to explain in a new way some characteristics of the effect of trimetazidine on human neutrophils and its effect in myocardial
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