Characterization of the effects of metabolic inhibitors, ATPase inhibitors and a potassium‐channel blocker on stomatal opening and closing in isolated epidermis of Commelina communis L.

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Abstract
The specific effects of hypoxia and various inhibitors on stomatal opening in the light and closing in the dark were characterized in isolated epidermis from Commelina communis L. Reducing the guard cell metabolism with hypoxia and the uncoupler carbonyl cyanide‐m‐chloro‐phenyl‐hydrazone, CCCP, respectively, inhibited both stomatal opening and closing. Stomatal closing was very efficiently blocked by CCCP and this effect could be readily reversed by washing out the inhibitor. The authors were unable to inhibit stomatal opening with ATPase‐inhibitors, without also affecting closing. Orthovanadate, up to 2 mol m−3, affected neither opening nor closing. Dicyclohexylcarbodiimide, DCCD, and diethylstilbestrol, DES, inhibited opening as well as closing to about 50%. The K+ ‐channel blocker tetraethylammonium chloride, TEA‐Cl, inhibited both stomatal opening and closing, as did phenyl acetic acid, PAA, a compound considered to interfere with blue light induced stomatal opening. The results are discussed in the view that the uncontrolled K+ leakage from the guard cells is low, that K+ efflux during stomatal closing, as well as K+ influx during opening, occurs through specific K+‐channels and that ATP and/or a membrane potential seems to be needed to keep these channels open.