Nifedipine (Procardia) is a dihydropyridine calcium channel blocking agent. Nifedipine inhibits the transmembrane influx of extracellular calcium ions into myocardial and vascular smooth muscle cells, causing dilatation of the main coronary and systemic arteries and decreasing myocardial contractility. This agent also inhibits the drug efflux pump P-glycoprotein which is overexpressed in some multi-drug resistant tumors and may improve the efficacy of some antineoplastic agents.

Nifedipine 显著增加了人类冠状动脉内皮细胞培养后的eNOS蛋白表达，这种增加与浓度相关。[1] Nifedipine 拮抗遍布心血管系统的L型Ca+通道，并且也能阻断Kv通道，Kv通道是同一超基因家族的成员。[2] Nifedipine 按剂量依赖性降低血管平滑肌细胞（VSMC）内[（3）H]-胸苷掺入量、总细胞蛋白含量以及磷酸化的细胞外信号调节蛋白激酶（ERK）1/2、丝裂原激活蛋白激酶激酶（MEK）1/2水平，甚至还降低了Pyk2的磷酸化水平。Nifedipine 还剂量依赖性地抑制VSMC和气球损伤胸主动脉中VSMC的增殖细胞核抗原（PCNA）水平。[3]

Nifedipine （3 mg/kg）可略微降低大鼠的收缩压或/和舒张压水平，或增加心率。[3] Nifedipine （1 μm）对脉络膜小动脉平滑肌的储存操作通路产生最大抑制作用。[4] Nifedipine （20 和 40 mg/kg）显著预防了HCl 加乙醇诱导的大鼠胃粘膜损伤以及损伤粘膜中硫代巴比妥酸反应物质含量的增加。Nifedipine （20 和 40 mg/kg）呈剂量依赖性地促进溃疡愈合并抑制溃疡粘膜中硫代巴比妥酸反应物质含量的增加。[5]

Cell viability is assessed using an MTT assay. Briefly, a total of 25 μL MTT (1 g/L in PBS) is added to each well before incubation is conducted at 37°C for 4 h. The assay is stopped by the addition of a 100 μL lysis buffer (20% SDS in 50% N'Ndimethylformamide, pH 4.7). Optical density (OD) is measured at the 570 nm wavelength by the use of an ELX-800 microplate assay reader and the results are expressed as a percentage of the absorbance measured in the control cells.