Nifedipine 是一种二氢吡啶类钙通道阻滞剂，可抑制细胞外钙离子跨膜流入心肌和血管平滑肌细胞，导致主要冠状动脉和全身动脉扩张，降低心肌收缩力。它常用于心肌功能不全的相关研究。

Nifedipine 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 causes a significant concentration-dependent increase in eNOS protein expression by cultured human coronary artery endothelial cells. [1] Nifedipine antagonizes L-type Ca+ channels found throughout the cardiovascular system, but also blocks Kv channels, which are members of the same supergene family. [2] Nifedipine dose-dependently decreases the values of [(3)H]-thymidine incorporation and total cellular protein content as well as the levels of phosphorylated extracellular signal-regulated protein kinase (ERK) 1/2, mitogen-activated protein kinase kinase (MEK) 1/2, and even the phosphorylation of Pyk2, in vascular smooth muscle cells (VSMC). Nifedipine suppresses the levels of proliferative cell nuclear antigen (PCNA) dose-dependently in both VSMC and balloon-injured thoracic aortae in VSMC. [3]

Nifedipine (3 mg/kg) slightly lowers the level of systolic and/or diastolic blood pressure or increased the heart rate in rats. [3] Nifedipine (1 μm) produces a maximal inhibition of the store-operated pathway in choroidal arteriolar smooth muscle. [4] Nifedipine (20 and 40 mg/kg) markedly prevents the HCl plus ethanol-induced gastric mucosal injury and the increase in the content of thiobarbituric acid-reactive substances in the injured mucosa in rats. Nifedipine (20 and 40 mg/kg) dose-dependently promotes the ulcer healing and inhibites the increase in the content of thiobarbituric acid-reactive substances in the ulcerated mucosa in rats. [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.

21829-25-4

C17H18N2O6

346.339

Procardia;硝苯地平;Procardia XL;BAY-a-1040;Adalat

Ethanol:12 mg/mL (34.6 mM)
DMSO:64 mg/mL (184.8 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years