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논문 기본 정보

자료유형
학술저널
저자정보
Park, Choon-Ok (Department of Physiology & the Cardiovascular Research Institute, Gyeongsang National University) So, In-Suk (Department of Physiology & the Heart Research Institute, Seoul National University College of Medicine) Ho, Won-Kyung (Department of Physiology & the Heart Research Institute, Seoul National University College of Medicine) Kim, Woo-Gyeum (Department of Physiology & the Heart Research Institute, Seoul National University College of Medicine) Earm, Yung-E (Department of Physiology & the Heart Research Institute, Seoul National University College of Medicine)
저널정보
대한생리학회 대한생리학회지 대한생리학회지 제26권 제1호
발행연도
1992.1
수록면
27 - 35 (9page)

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We used the whole cell patch clamp technique to examine the ionic basis for the tail current after depolarizing pulse in single atrial myocytes of the rabbit. We recorded the tail currents during various repolarizations after short depolarizing pulse from a holding potential of -70 mV. The potassium currents were blocked by external 4-aminopyridine and replacement of internal potassium with cesium. The current was reversed to the outward direction above +10 mV. High concentrations of intracellular calcium buffer inhibited the activation of the current. Diltiazem and ryanodine blocked it too. These data suggest that the current is activated by intracellular calcium released from sarcoplasmic reticulumn. When the internal chloride concentration was increased, the inward tail current was increased. The current was partially blocked by the anion transport blocker niflumic acid. The current voltage curve of the niflumic acid sensitive current component shows outward rectification and is well fitted to the current voltage curve of the theoretically predicted chloride current calculated from the constant field equation. The currents recorded in rabbit atrial myocytes, with the method showing isolated outward Na Ca exchange current in ventricular cells of the guinea pig, suggested that chloride conductance could be activated with the activation of Na/ca exchange current. From the above results it is concluded that a chloride sensitive component which is activated by intracellular calcium contributes to tail currents in rabbit atrial cells.

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