Abstract
The action of a wide range of drugs effective on Ca2+ channels in animal tissues has been measured on Ca2+ 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 Ca2+ 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 Ca2+ influx. Conversely, bepridil greatly and irreversibly stimulated Ca2+ influx, and with time, stopped cytoplasmic streaming (which is sensitive to increases in cytoplasmic Ca2+). By apparently altering the cytoplasmic Ca2+ levels with various drugs, it was found that (with the exception of the inorganic cation, La3+) treatments likely to lead to an increase in cytoplasmic Ca2+ levels caused an increase in the rate of closure of the K+ channels. Similarly, treatments likely to lead to a decrease in cytoplasmic Ca2+ 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 Ca2+, 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 Ca2+, with increased free Ca2+ levels leading to an increased rate of K+-channel closure. As well as inhibiting Ca2+ channels, it is suggested that La3+ acts on a Ca2+-binding site of the K+ channel, mimicking the effect of Ca2+ and increasing the rate of channel closure.