Calcium channel and calcium pump involved in oscillatory hyperpolarizing responses of L‐strain mouse fibroblasts

1. In fibroblastic L cells, spontaneously repeated hyperpolarizing responses (oscillation of membrane potential) and hyperpolarizing responses evoked by electrical stimuli were suppressed by the external application of a K + channel blocker, nonyltriethylammonium (C 9 ). This hydrophobic TEA‐analogue also inhibited the hyperpolarization induced by intracellular Ca 2+ injection. 2. Quinine or quinidine, known inhibitors of the Ca 2+ ‐activated K + channel of red cells, instantaneously inhibited these hyperpolarizations. Thus, these hyperpolarizations are likely to be caused by the operation of Ca 2+ ‐sensitive K + channels. 3. Azide, which is known to inhibit the mitochondrial Ca 2+ uptake in fibroblasts, and caffeine, dantrolene Na and oxalate, which affect the microsomal Ca 2+ transport, did not exert any effects upon the electrical potential profiles. 4. On the other hand, Ca 2+ channel blockers (nifedipine, D 600 and Co 2+ ) suppressed the hyperpolarizing responses, but not the hyperpolarizations produced by intracellular Ca 2+ injection, suggesting that the calcium ions responsible for the hyperpolarizing responses are mainly derived from outside the cell through Ca 2+ channels. 5. Flavones of plant origin, which are known to inhibit Ca 2+ ‐ATPase, prolonged the duration of the hyperpolarizing phase of the oscillation or produced a sustained hyperpolarization. 6. It is concluded that the Ca 2+ channel and the Ca 2+ pump play essential roles in the generation of the hyperpolarizing response and of the membrane potential oscillation in L cells, and that these hyperpolarizations are brought about by a transient elevation of cytosolic Ca 2+ level which, in turn, activates Ca 2+ ‐dependent K + channels.