In various plant materials changes in turgor pressure, following hyper- or hypo-osmotic stress, were associated with the activation or inactivation of the plasma membrane H⁺ -ATPase, respectively. To see if the turgor changes might indirectly influence H⁺ -ATPase activity by regulating ion fluxes through plasma membrane, we investigated, in cultured cells of Arabidopsis thaliana (L.) Heynh., the early effects of hyper- and hypo-osmotic stress on Cl^- fluxes in comparison, in the case of hyper-osmotic treatment, with its effect on net H⁺ extrusion. The results obtained showed that hyper-osmotic stress (200 mM mannitol) quickly reduced Cl^- efflux (-70%) from cells preloaded with ³⁶ C1^- for 18 h. This inhibiting effect was independent of the simultaneous mannitol-induced stimulation of Cl^- influx and rapidly reversible after removal of the hyper-osmotic treatment. The inhibition of Cl^- efflux was associated with a stimulation of net H⁺ extrusion, and these two effects showed the same dependence on the external mannitol concentration. Fusicoccin (FC, 20 µM), which stimulated H⁺ extrusion to about the same extent as 200 mM mannitol, did not affect Cl^- efflux. When cells preloaded with ³⁶ C1^- for 18 h in the presence of mannitol (from 25 up to 200 mM) were eluted in a mannitol-free medium an early and strong increase in Cl^- efflux was found. The increase of Cl- efflux was already detectable for a small hypo-osmotic jump (25 mM), and was reduced (-50%) by the anion channel inhibitor A9C (300 µM). These results lead to exclude a direct causal relationship mediated by E_m changes between the effects of osmoticum on Cl^- efflux and net H⁺ extrusion, and favour the view that the changes in turgor pressure induced by hyper/hypo-osmotic stress may respectively induce an early inactivation/activation of stretch-sensitive anion channels.

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