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Nifedipine (BAY-a-1040) is a potent calcium channel blocker and drug of choice for cardiac insufficiencies.

Nifedipine (BAY-a-1040) (100 μM) significantly lowers the viability of the WKPT-0293 Cl.2 Cells, and treatment of nifedipine (10 or 100 μM) plus FAC induces a significant reduction in cell viability, but there are no significant differences in viability between the control cells and the cells treated with 100 μM of FAC or 1 and 10 μM of nifedipine.Nifedipine (BAY-a-1040) (1, 10, or 100 μM) significantly increases iron level in WKPT-0293 Cl.2 cells. Nifedipine treatment also increases expression of TfR1, DMT1+IRE and DMT1-IRE in WKPT-0293 Cl.2 cells. In addition, co-treatment with nifedipine (100 μM) and FAC (100 μM) increases TfR1, DMT1+IRE and DMT1-IRE expression in WKPT-0293 Cl.2 cells[2]. Nifedipine plus ritodrine produces a significantly greater inhibition of contractility than each drug alone in the midrange of concentrations. The combination of nifedipine plus nitroglycerin or nifedipine plus atosiban produces a significantly greater inhibition than nitroglycerin or atosiban alone but not greater than nifedipine. The combination of nifedipine plus NS-1619 (Ca2+-activated K+ [BKCa] channel opener) reduces the inhibitory effect of each drug[3]. Nifedipine (BAY-a-1040) (2 μM) significantly inhibits P. capsici mycelial growth and sporulation. Nifedipine (BAY-a-1040)-induced inhibition of mycelial growth is calcium-dependent. Nifedipine (0.5 μM) increases P. capsici sensitivity to H2O2 in a calcium-dependent manner. Nifedipine inhibition of P. capsici virulence and expression of genes involved in pathogenicity[4].

In Nifedipine (BAY-a-1040) (50 mg/kg)- and CsA-treated rats, the BL dimensions (BLi and BLk), MD dimensions (MDk) and vertical dimensions (VHi and VHk) are significantly increased (P < 0.05) at the end of the 4th week[1].

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