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HCO₃^– Influx across the Plasmalemma of Chara corallina ¹

Physiological and Biophysical Influence of 10 mM K⁺

Roger M. Spanswick

Jack Dainty

Department of Botany, University of California, Davis, California 95616, Division of Biological Sciences, Cornell University, Ithaca, New York 14853, Department of Botany, University of Toronto, Toronto, Ontario, M5S 1A1, Canada

The effect of 10 mM K⁺ on the HCO₃^– influx in Chara corallina has been used to distinguish a Ca²⁺-dependent membrane integrity site from the HCO₃^– transport site which is also Ca²⁺-dependent (Lucas and Dainty, Plant Physiology 1977 60: 862-867).

In the presence of 0.2 mM Ca²⁺ at pH 9, 10 mM K⁺ inhibits the HCO₃^– influx and depolarizes the membrane potential. Inhibition of the HCO₃^– influx may be prevented by raising the Ca²⁺ concentration in the solution or by addition of Mg²⁺, Sr²⁺, or Mn²⁺. Protection is also afforded by 20 mM Na⁺ and Cs⁺ but not by Rb⁺ which acts as a weak analog of K⁺ in producing inhibition of the HCO₃^– influx and depolarization of the membrane potential. With the exception of Na⁺, ions which prevent inhibition of the influx also prevent depolarization of the membrane potential.

Once inhibited by 10 mM K⁺, HCO₃^– transport cannot be restored by addition of Ca²⁺, Mg²⁺, or Sr²⁺ in less than 3 hours. Addition of Mn²⁺, however, results in a progressive restoration of the proportion of cells with influxes equal to the control value. Mn²⁺ also produces an increase in the membrane potential with a sharp hyperpolarization occurring at a threshold of about—180 mv. This sudden recovery of the HCO₃^– influx in individual cells contrasts with the gradual recovery observed when the K⁺ concentration is reduced to 0.2 mM. Since Mn²⁺ cannot substitute for Ca²⁺ at the HCO₃^– transport site, restoration of HCO₃^– transport by Mn²⁺ involving the membrane integrity site, as evidenced by the effect on the membrane potential and resistance, is clearly separate. The other divalent cations were able to restore HCO₃^– transport if applied at a concentration of 2 mM for 14 hours.

The OH^– efflux is also inhibited by 10 mM KCl. It is postulated that voltage dependency of the OH^– or HCO₃^– transport systems may account for the observed effects of 10 mM K⁺ on the HCO₃^– influx.