• Korean Journal of Veterinary Research
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• v.34 no.1
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• pp.25-36
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• 1994

The inward tail current after a short depolarizing pulse has been known as Na-Ca exchange current activated by intracellular calcium which forms late plateau of the action potential in rabbit atrial myocytes. Chloride conductance which is also dependent upon calcium concentration has been reported as a possible tail current in many other excitable tissues. Thus, in order to investigate the exsitance of the calcium activated chloride current and its contribution to tail current, whole cell voltage clamp measurement has been made in single atrial cells of the rabbit. The current was recorded during repolarization following a brief 2 ms depolarizing pulse to +40mV from a holding potential of -70mV. When voltage-sensitive transient outward current was blocked by 2 mM 4-aminopyridine or replacement potassium with cesium, the tail current were abolished by ryanodine$(1{\mu}M)$ or diltiazem$(10{\mu}M)$ and turned out to be calcium dependent. The magnitudes of the tail currents were increased when intracellular chloride concentration was increased to 131 mM from 21 mM. The current was decreased by extracellular sodium reduction when intracellular chloride concentration was low(21 mM), but it was little affected by extracellular sodium reduction when intracellual chloride concentration was high(131 mM). The current-voltage relationship of the difference current before and after extracellular sodium reduction, shows an exponential voltage dependence with the largest magnitude of the current occurring at negative potentials, with is similar to current-voltage relationship at negative potentials, which is similar to current-voltage relationship of Na-Ca exchange current. The current was also decreased by $10{\mu}M$ niflumic acid and 1 mM bumetanide, which is well known anion channel blockers. The reversal potentials shifted according to changes in chloride concentration. The current-voltage relationships of the niflumic acid-sensitive currents in high and low concentration of chloride were well fitted to those predicted as chloride current. From the above results, it is concluded that calcium activated chloride component exists in the tail current with Na-Ca exchange current and it shows the reversal of tail current. Therefore it is thought that in the physiologic condition it leads to rapid end of action potential which inhibits calcium influx and it contributes to maintain the low intracellular calcium concentration with Na-Ca exchange mechanism.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.6
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• pp.335-338
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• 2004

There are numerous studies on transepithelial transports in duct cells including $Cl^-$ and/or $HCO_3^-$. However, studies on transepithelial $K^+$ transport of normal duct cells in exocrine glands are scarce. In the present study, we examined the characteristics of $K^+$ currents in single duct cells isolated from guinea pig pancreas, using a whole-cell patch clamp technique. Both $Cl^-$ and $K^+$ conductance were found with KCI rich pipette solutions. When the bath solution was changed to low $Cl^-$, reversal potentials shifted to the negative side, $-75{\pm}4\;mV$, suggesting that this current is dominantly selective to $K^+$. We then characterized this outward rectifying $K^+$ current and examined its $Ca^{2+}$ dependency. The $K^+$ currents were activated by intracellular $Ca^{2+}$. 100 nM or 500 nM $Ca^{2+}$ in pipette significantly (P<0.05) increased outward currents (currents were normalized, $76.8{\pm}7.9\;pA$, n=4 or $107.9{\pm}35.5\;pA$, n=6) at +100 mV membrane potential, compared to those with 0 nM $Ca^{2+}$ in pipette $(27.8{\pm}3.7\;pA,\;n=6)$. We next examined whether this $K^+$ current, recorded with 100 nM $Ca^{2+}$ in pipette, was inhibited by various inhibitors, including $Ba^{2+}$, TEA and iberiotoxin. The currents were inhibited by $40.4{\pm}%$ (n=3), $87.0{\pm}%$ (n=5) and $82.5{\pm}%$ (n=9) by 1 mM $Ba^{2+}$, 5 mM TEA and 100 nM iberiotoxin, respectively. Particularly, an almost complete inhibition of the current by 100 nM iberiotoxin further confirmed that this current was activated by intracellular $Ca^{2+}$. The $K^+$ current may play a role in secretory process, slnce recycling of $K^+$ is critical for the initiation and sustaining of $CI^-$ or $HCO_3^-$ secretion in these cells.