Recent studies fail to confirm the coexistence of Na+ channels and Na/H+ exchange at the apical membranes of lower airway epithelia. Availa
bility of plasma membrane vesicles simplifies the investigation of mem
brane transport processes. Apical and basolateral plasma membrane vesi
cles of disrupted type-II pneumocytes were fractionated upon nonlinear
, continuous sucrose gradients. To investigate sodium transport, Na-22
+ uptake by apical membrane vesicles was assayed in the presence and a
bsence of transmembrane sodium diffusion potentials. Interior-negative
sodium diffusion potentials promoted Na-22+ uptake 1.5-fold. Internal
ly-directed H+ gradients or NH4+ gradients inhibited Na-22+ uptake 40-
50%. Amiloride (1-1000 muM) inhibited uptake 10-79%. To investigate H transport, decay of transmembrane pH gradients was monitored with pH
probe acridine orange. In the presence or absence of externally-direct
ed H+ gradients, external sodium promoted internal alkalinization, exc
ept in the presence of external amiloride. These observations of amilo
ride-sensitive, electrogenic Na+ uptake and amiloride-sensitive, elect
roneutral, Na+/H+ coupling indicate coexistence of Na+ channels and Na
+/H+ exchange at the apical membrane of type-II pneumocytes.