In isolated Elodea densa leaves, the relationships between H+ extrusion (-Delta H+), K+ fluxes and membrane potential (E(m)) were investigated for two different conditions of activation of the ATP-dependent H+ pump. The 'basal condition' (darkness, no pump activator present) was characterized by low values of -Delta H+ and K+ uptake (Delta K+), wide variability of the -Delta H+/Delta K+ ratio, relatively low membrane polarization and E(m) values more positive than E(K) for external K+ concentrations ([K+](0)) of up to 2 mol m(-3). A net K+ uptake was seen already at [K+](0) below 1 mol m(-3), suggesting that K+ influx in this condition was a therm modynamically uphill process involving an active mechanism, When the H+ pump was stimulated by fusicoccin (FC), by cytosol acidification, or by light (the 'high polarization condition'), K+ influx largely dominated K+ and Cl- efflux, and the -Delta H+/Delta K+ ratio approached unity, In the range 50 mmol m(-3) -5 mol m(-3) [K+](0), E(m) was consistently more negative than E(K). The curve of K+ influx at [K+](0) ranging from 50 to 5000 mmol m(-3) fitted a monophasic, hyperbolic curve, with an apparent half saturation value = 0.2mol m(-3). Increasing [K+](0) progressively depolarized E(m), counteracting the strong hyperpolarizing effect of FC. The effects of K+ in depolarizing E(m) were well correlated with the effects on both K+ influx and -Delta H+, suggesting a cause-effect chain: K-0(+) influx --> depolarization --> activation of H+ extrusion, Cs+ competitively inhibited K+ influx much more strongly in the 'high polarization' than in the 'basal' condition (50% inhibition at [Cs+]/[K+](0) ratios of 1:14 and 1:2, respectively) thus confirming the involvement of different K+ uptake systems in the two conditions, These results suggest that in E. densa leaves two distinct modes of interactions rule the relationships between H+ pump, membrane polarization and K+ transport, At low membrane polarization, corresponding to a low state of activation of the PM H+-ATPase and to E(m) values more positive than E(K), K+ influx would mainly depend on an active transport mechanism, whereas in the condition of high activation of the H+-ATPase and of E(m) more negative than E(K) the hyperpolarization-activated voltage-gated K+ channels would become the dominant system for passive K+ influx, even at very low, micromolar extracellular K+ concentrations. The linkage between H+-ATPase and K+ fluxes would depend mainly (although not exclusively) on the interplay between hyperpolarization by the H+ pump, controlling voltage-gated K+ channels, and depolarization by K+ net uptake, facilitating H+ extrusion by the pump.
