Cytoplasmic calcium affects the gating of potassium channels in the plasma membrane ofChara corallina: a whole-cell study using calcium-channel effectors.

The action of a wide range of drugs effective on Ca(2+) channels in animal tissues has been measured on Ca(2+) channels open during the action potential of the giant-celled green alga,Chara corallina. Of the organic effectors used, only the 1,4-dihydropyridines were found to inhibit reversibly Ca(2+) influx, including, unexpectedly, Bay K 8644 and both isomers of 202-791. Methoxyverapamil (D-600), diltiazem, and the diphenylbutylpiperidines, fluspirilene and pimozide were found not to affect the Ca(2+) influx. Conversely, bepridil greatly and irreversibly stimulated Ca(2+) influx, and with time, stopped cytoplasmic streaming (which is sensitive to increases in cytoplasmic Ca(2+)). By apparently altering the cytoplasmic Ca(2+) levels with various drugs, it was found that (with the exception of the inorganic cation, La(3+)) treatments likely to lead to an increase in cytoplasmic Ca(2+) levels caused an increase in the rate of closure of the K(+) channels. Similarly, treatments likely to lead to a decrease in cytoplasmic Ca(2+) decreased the rate of K(+) channel closure. The main effect of bepridil on the K(+) channels was to increase the rate of voltage-dependent channel closure. The same effect was obtained upon increasing the external concentration of Ca(2+), but it is likely that this was due to effects on the external face of the K(+) channel. Addition of any of the 1,4-dihydropyridines had the opposite effect on the K(+) channels, slowing the rate of channel closure. They sometimes also reduced K(+) conductance, but this could well be a direct effect on the K(+) channel; high concentrations (50 to 100 μM) of bepridil also reduced K(+) conductance. No effect of photon irradiance or of abscisic acid could be consistently shown on the K(+) channels. These results indicate a control of the gating of K(+) channels by cytoplasmic Ca(2+), with increased free Ca(2+) levels leading to an increased rate of K(+)-channel closure. As well as inhibiting Ca(2+) channels, it is suggested that La(3+) acts on a Ca(2+)-binding site of the K(+) channel, mimicking the effect of Ca(2+) and increasing the rate of channel closure.