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본문내용
ery smooth muscle cells. Voltage-operated Ca2+ channel current was recorded, and it could contribute to the increase in the intracellular Ca2+ concentration in the case of the membrane depolarization. The intracellular Ca2+ store was also well developed. The extracellular application of the caffeine or histamine increased the intracellular Ca2+ concentration.
We recorded the Ca2+-activated current induced by the application of the 5 mM caffeine. The main component of the caffeine-induced Ca2+-activated currents was considered to be Ca2+-activated K+ current, since the reversal potential of the current was near the K+ equilibrium potential. But some inward currents also seemed to be activated by intracellular Ca2+ increase. For the investigation of the current other than Ca2+-activated K+ current, we used K+-free intracellular and extracellular solutions. In this condition, the total replacement of the extracellular Na+ with NMDG+ or Cs+ affected little to the inward component and reversal potential of the Ca2+-activated currents. This indicates that non-selective cation current was not activated by the increased intracellular Ca2+ concentration. The Ca2+-activated current in the K+-free condition was completely inhibited by the bath application of the 100 μM niflumic acid. And the reduction of the extracellular NaCl concentration from the 152 mM NaCl to 72 mM shifted the reversal potential of the Ca2+-activated current to that of the Cl- ion. This implies that the Ca2+-activated current in K+-free condition is Ca2+-activated Cl- current. We replaced the extracellular Na+ with Li+ whilst measuring intracellular Ca2+. The total replacement of the extracellular Na+ with Li+ did not slowed the decay rate of the Ca2+ transient induced by the caffeine. This shows that Na+/Ca2+ exchanger is not functional and cannot generate Na+/Ca2+ exchanger current in the case of the intracellular Ca2+ increase.
In summary, there presents VOCC, which contribute to the intracellular Ca2+ increase in the case of membrane depolarization, and intracellular Ca2+ store, which releases Ca2+ to the cytoplasmic side in the case of some agonists application in the pulmonary artery smooth muscle cell of the rabbit. The Ca2+-activated current was mainly composed of the Ca2+-activated K+ current and Cl- current. Ca2+-activated non-selective cation current and Na+/Ca2+ exchanger current were not detected. The relative Ca2+ sensitivity and capacity of the Ca2+-activated K+ current and Cl- current seem to be important aspect in regulating the excitability of the pulmonary artery smooth muscle since they take part in the regulation of the excitability in opposite way of feedback mechanism(Ca2+-activated K+ current in negative feedback mechanism and Cl- current in positive feedback mechanism, respectively).
keywords : pulmonary artery smooth muscle, intracellular Ca2+, Ca2+-activated ion channel, Na+-Ca2+ exchanger, negative/positive feedback regulation
Student Number : 91801-837
We recorded the Ca2+-activated current induced by the application of the 5 mM caffeine. The main component of the caffeine-induced Ca2+-activated currents was considered to be Ca2+-activated K+ current, since the reversal potential of the current was near the K+ equilibrium potential. But some inward currents also seemed to be activated by intracellular Ca2+ increase. For the investigation of the current other than Ca2+-activated K+ current, we used K+-free intracellular and extracellular solutions. In this condition, the total replacement of the extracellular Na+ with NMDG+ or Cs+ affected little to the inward component and reversal potential of the Ca2+-activated currents. This indicates that non-selective cation current was not activated by the increased intracellular Ca2+ concentration. The Ca2+-activated current in the K+-free condition was completely inhibited by the bath application of the 100 μM niflumic acid. And the reduction of the extracellular NaCl concentration from the 152 mM NaCl to 72 mM shifted the reversal potential of the Ca2+-activated current to that of the Cl- ion. This implies that the Ca2+-activated current in K+-free condition is Ca2+-activated Cl- current. We replaced the extracellular Na+ with Li+ whilst measuring intracellular Ca2+. The total replacement of the extracellular Na+ with Li+ did not slowed the decay rate of the Ca2+ transient induced by the caffeine. This shows that Na+/Ca2+ exchanger is not functional and cannot generate Na+/Ca2+ exchanger current in the case of the intracellular Ca2+ increase.
In summary, there presents VOCC, which contribute to the intracellular Ca2+ increase in the case of membrane depolarization, and intracellular Ca2+ store, which releases Ca2+ to the cytoplasmic side in the case of some agonists application in the pulmonary artery smooth muscle cell of the rabbit. The Ca2+-activated current was mainly composed of the Ca2+-activated K+ current and Cl- current. Ca2+-activated non-selective cation current and Na+/Ca2+ exchanger current were not detected. The relative Ca2+ sensitivity and capacity of the Ca2+-activated K+ current and Cl- current seem to be important aspect in regulating the excitability of the pulmonary artery smooth muscle since they take part in the regulation of the excitability in opposite way of feedback mechanism(Ca2+-activated K+ current in negative feedback mechanism and Cl- current in positive feedback mechanism, respectively).
keywords : pulmonary artery smooth muscle, intracellular Ca2+, Ca2+-activated ion channel, Na+-Ca2+ exchanger, negative/positive feedback regulation
Student Number : 91801-837
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