Abaxial and adaxial stomatal responses to benzo-18-crown-6 (a synthetic K+ ionophore), alone and in combination with abscisic acid (ABA), were examined on isolated epidermes of Commelina communis. Increasing ionophore concentration progressively suppressed abaxial opening, while up to an optimum concentration it enhanced adaxial opening although higher concentrations caused closure; stomatal K+ changed correspondingly. Increasing KCl progressively alleviated the ionophore-induced closure. The effects of the ionophore and ABA were strongly antagonistic. Benzo-18-crown-6 is postulated to eliminate an inherent disparity in permeability to K+ between the membranes of abaxial and adaxial guard cells by making them more permeable. In normal abaxial functioning a net K+ gain promotes wide opening, but the ionophore-enhanced permeability results in a net K+ loss causing closure, because the intensified efflux down a concentration gradient outweighs the influx driven by a proton pump. The normally low adaxial K+ accumulation is attributed to an inherently restricted membrane permeability which benzo-18-crown-6 is postulated to alleviate progressively with increasing concentration; an enhanced permeability up to an optimum level allows a net K+ gain producing wide apertures, but any further increase in permeability leads to a net K+ loss, like that in abaxial guard cells, causing closure. The progressive reduction of the ionophore-induced closure with increasing external KCl supply and the strong antagonistic interaction between the ionophore and ABA support this postulation. The results suggest that the normal disparity in abaxial and adaxial opening is linked specifically with differential K+ accumulation in the guard cells.