In vitro activity: Felodipine significantly relaxes KCl-contracted porcine coronary segments by blocking the Ca2+ channels, displaying ~50 times more potent than nifedipine (IC50 of ~8 nM) and ~430 times than verapamil (IC50 of ~65 nM). Felodipine significantly induces the transcription and secretion of IL-6 and IL-8 with ED50 values of 5.8 nM and 5.3 nM in primary human VSMC and lung fibroblasts, respectively, while propranolol or furosemide fails to affect the expression of the two IL genes. Felodipine blocks the muscarinic receptor-mediated (carbachol) Ca2+-dependent contraction of guinea pig ileum longitudinal smooth muscle (GPILSM) with an IC50 of 1.45 NM. Felodipine at low concentration of 0.1 μM is sufficient to increases NOx generation, Ca2+-dependent NOS activity, and eNOS protein mass in rat endothelial cells. Felodipine (10 μM) reduces nuclear translocation of p42/44 mitogen-activated protein kinase and Elk-1 activation stimulated by PDGF-BB, leading to the inhibition of human SMC proliferation. Felodipine modestly blocks the Cav3.2 T-type Ca2+-channel with an IC50 of 6.8 μM.

Cell Assay: felodipine significantly induces the transcription and secretion of IL-6 and IL-8 with ED50 values of 5.8 nM and 5.3 nM in primary human VSMC and lung fibroblasts, respectively, while propranolol or furosemide fails to affect the expression of the two IL gene

J Pharmacol Exp Ther. 1983 Aug;226(2):330-4; J Mol Cell Cardiol. 1995 Oct;27(10):2295-302.