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.
D000818:Animals; D001693:Biological Transport, Active; D002118:Calcium / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005419:Flavonoids / Q000494:pharmacology; D007473:Ion Channels / Q000502:physiology*; D007739:L Cells / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009543:Nifedipine / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D011802:Quinidine / Q000494:pharmacology; D011803:Quinine / Q000494:pharmacology
D005419:Flavonoids; D007473:Ion Channels; D011803:Quinine; D009543:Nifedipine; D011802:Quinidine; D011188:Potassium; D002118:Calcium