Biomedicine (Taipei). 2014;4:24. doi: 10.7603/s40681-014-0024-z. Epub 2014 Nov 18.
BioMedicine
Tz-Chong Chou
PMID: 25520937 PMCID: PMC4265014 DOI: 10.7603/s40681-014-0024-z
Platelet hyperactivity often occursd in hypertensive patients and is a key factor in the development of cardiovascular diseases including thrombosis and atherosclerosis. Nifedipine, an L-type calcium channel blocker, is widely used for hypertension and coronary heart disease therapy. In addition, nifedipine is known to exhibit an antiplatelet activity, but the underlying mechanisms involved remain unclear. Several transcription factors such as peroxisome proliferator-activated receptors (PPARs) and nuclear factor kappa B (NF-κB) exist in platelets and have an ability to regulate platelet aggregation through a non-genomic mechanism. The present article focuses on describing the mechanisms of the antiplatelet activity of nifedipine
Keywords: Nifedipine; Nitric oxide; Nuclear factor-κB; Peroxisome; Platelet aggregation; Protein kinase Cα; proliferator-activated; receptors