Bidani A, Heming T A
Department of Internal Medicine, University of Texas Medical Branch, Galveston 77555-0876, USA.
Lung. 1998;176(1):25-34. doi: 10.1007/pl00007589.
Alveolar macrophages (m phi) possess two parallel mechanisms for plasmalemmal H+ extrusion: a V-type H+ pump (V-ATPase) and a Na+/H+ exchanger (NHE). To investigate the coordinated functioning of the H+ extruders for m phi intracellular pH (pHi) regulation, we investigated the effects of the plant lectin concanavalin A (ConA) on resident alveolar m phi from rabbits. ConA (1 microM, 30-min pretreatment) activated the m phi for phagocytosis of opsonized Escherichia coli. ConA activation did not affect the baseline pHi of m phi or the initial rate of pHi recovery (dpHi/dt) from an intracellular acid load (acid-loaded pHi nadir approximately 6.9). However, the contributions of Na(+)-independent H+ transport (i.e. V-ATPase activity) and Na(+)-dependent H+ transport (i.e. NHE activity) to dpHi/dt were altered significantly. The lectin stimulated Na+/H+ exchange and inhibited V-ATPase activity. In control m phi, V-ATPase-mediated H+ extrusion was responsible for > 80% of dpHi/dt. Conversely, in ConA-treated m phi, Na+/H+ exchange was responsible for approximately 65% of dpHi/dt, and V-ATPase activity was responsible for only 35% of dpHi/dt. These results underscore the complex mechanisms and signaling pathways that coordinate the activities of cellular acid-base transporters in m phi pHi regulation.
