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Department of Physiology, Faculty of Medicine, Kyoto University, Kyoto 606, Japan

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 (C₉). This hydrophobic TEA-analogue also inhibited the hyperpolarization induced by intracellular Ca²⁺ injection.

2. Quinine or quinidine, known inhibitors of the Ca²⁺-activated K⁺ channel of red cells, instantaneously inhibited these hyperpolarizations. Thus, these hyperpolarizations are likely to be caused by the operation of Ca²⁺-sensitive K⁺ channels.

3. Azide, which is known to inhibit the mitochondrial Ca²⁺ uptake in fibroblasts, and caffeine, dantrolene Na and oxalate, which affect the microsomal Ca²⁺ transport, did not exert any effects upon the electrical potential profiles.

4. On the other hand, Ca²⁺ channel blockers (nifedipine, D 600 and Co²⁺) suppressed the hyperpolarizing responses, but not the hyperpolarizations produced by intracellular Ca²⁺ injection, suggesting that the calcium ions responsible for the hyperpolarizing responses are mainly derived from outside the cell through Ca²⁺ channels.

5. Flavones of plant origin, which are known to inhibit Ca²⁺-ATPase, prolonged the duration of the hyperpolarizing phase of the oscillation or produced a sustained hyperpolarization.

6. It is concluded that the Ca²⁺ channel and the Ca²⁺ 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 Ca²⁺ level which, in turn, activates Ca²⁺-dependent K⁺ channels.

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				J. P. Grierson and J. Meldolesi Shear Stress-induced [Ca[IMAGE]][IMAGE] Transients and Oscillations in Mouse Fibroblasts Are Mediated by Endogenously Released ATP J. Biol. Chem., March 3, 1995; 270(9): 4451 - 4456. [Abstract] [Full Text] [PDF]