Nifedipine impairs neutrophil respiratory burst by a mechanism other than calcium channel blockade.

Superoxide production by mice neutrophils was inhibited by nifedipine exposure in a dose dependent manner. The inhibition of Ca2+ uptake elicited by nifedipine did not appear to account for the observed effect as the extracellular Ca2+ enrichment and depletion did not produce a significant reversal of the inhibition. Cytosolic free Ca2+ as measured by Quin 2AM fluorescence did not show any significant change, indicating that the effect was independent of the inhibition of Ca2+ influx. In addition nifedipine caused a significant inhibition (p less than 0.01) in NADPH oxidase activity. Our data indicates that nifedipine inhibits superoxide production independent of inhibiting Ca2+ inflow and supports the hypothesis that Ca2+ antagonists affect cellular functions by non Ca2+ mediated process as well.