Abstract
We examined the role of the monovalent cations Na^+^ and K^+^ in the events encompassing the release of O by alveolar macrophages after stimulation with formyl methionyl phenylalanine (FMP). This was accomplished by determining the effect of changing the extracellular [Na^+^] and/or [K^+^] on FMP‐stimulated O production; and measuring ^22^Na^+^ ^42^K^+^ and ^86^Rb^+^ influx and efflux and intracellular [K^+^] for control and FMP‐stimulated alveolar macrophages. Stimulated O production was relatively insensitive to changes in extracellular K^+^ or Na^+^ concentrations until the [Na^+^] was decreased below 35 mM. At 4 mM [Na^+^], the rate of O production remained at 75% of the maximal rate observed at physiological concentrations of [Na^+^]. Both influx and efflux of ^22^Na^+^ were stimulated above control rates by FMP. The increased rates of fluxes lasted for a few minutes suggesting a transient increase in membrane permeability to Na^+^. Ouabain partially inhibited ^22^Na^+^ efflux but had no effect on O release. The influx of ^86^Rb^+^ and ^42^K^+^ was not altered by the addition of FMP but was virtually abolished in the presence of 10 μM ouabain or 1 mM quinine. In the presence of extracellular calcium, FMP‐stimulated a prolonged (> 20 minutes) increase in ^86^Rb^+^ or ^42^K^+^ efflux which was inhibitable by 1 mM quinine. In the absence of extracellular calcium, FMP stimulation of K^+^ efflux was greatly diminished and was not affected by quinine, although quinine still inhibited O production under these conditions. It was also observed that there was a loss of intracellular K^+^ when cells were stimulated by FMP in the presence of Ca^+2^, but not in the absence of Ca^+2^. Taken together, these results suggest a minimal direct role, if any, for K^+^ in the events that lead to FMP‐stimulated O release by alveolar macrophages.