Purpose of review: Researchers and physicians are gaining more understanding of the utility of calcium channel blockers (CCBs) especially in modulation of innate immunity, and choose suitable ones in clinical practice. This review summarizes the recent related research findings.
Recent findings: Sustained and/or dysregulated expression of pro-inflammatory cytokines is sufficient to produce tissue injury and provoke overt cardiac decompensation. The important question that remains to be addressed is whether or not it will be possible to modulate the inappropriate or maladaptive consequences of innate immune activation and pro-inflammatory cytokine expression in the mammalian heart. CCBs, such as nifedipine, amlodipine, diltiazem, and verapamil, promote the relaxation of cardiac and smooth muscle cells by inhibiting calcium influx through calcium channels and calcium release from intracellular stores, and are commonly used in the treatment of cardiovascular disorders. Recently, several in-vitro studies have shown that, besides the effects they exert on muscle cells, CCBs also suppress the activation of various participants in immune reactions, including T cells, mast cells and macrophages, suggesting that they can be immunosuppressant.
Summary: CCBs maybe suppress the activation of various participants in immune reactions.