SUMMARY
The effects of varying concentrations of phenylacetic acid (PAA), alone and in combination with abscisic acid (ABA), on abaxial and adaxial stomatal movements were examined on isolated epidermis of Commelina communis. Increasing PAA concentration progressively suppressed abaxial opening, while up to 5 mol m−3 PAA produced remarkably wide adaxial apertures but higher concentrations caused closure; the stomatal K.+ changed accordingly. PAA, like the K+ ionophore benzo‐18‐crown‐6, showed strong antagonistic interactions with ABA. The results are interpreted by postulating that PAA, like benzo‐18‐crown‐6, increases the membrane permeability to K+. The normal abaxial permeability allows a net K+ gain required for opening, but the PAA‐induced increase in permeability causes a net K+ loss leading to closure, because the efflux down a concentration gradient outweighs the influx coupled with proton extrusion. In contrast, the normal K+ content is much less in adaxial than in abaxial guard cells, clear evidence of an inherent restriction to K+ fluxes; this is attributed to restricted membrane permeability to K+, which PAA is postulated to alleviate progressively with increasing concentration. Thus, an increase in permeability up to a critical limit favours a net K+ gain and promotes opening, but any further increase leads to a net K+ loss and causes closure, as in abaxial guard cells. This interpretation is substantiated by both the progressive reduction of PAA‐induced closure with increasing KC1 in the medium and the close similarity of the effects of PAA and benzo‐18‐crown‐6, alone and in antagonism with ABA, on abaxial and adaxial stomata.