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KMID : 0374919950160010091
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Inje Medical Journal
1995 Volume.16 No. 1 p.91 ~ p.106
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The Study of ATP-Sensitive K Channel in Rabbit Ventricular Myocytes
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Abstract
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To estimate the propertis of KATP channels and their modulation by intracellular and extracellular factors. rabbit ventricular myocytes were voltage and current clamped by a conventional patch clamp method at temperature of 37℃ or 27℃.
Metabolic inhibitionwas simulated by either application of metabolic inhibitor (2,4-dinitrophenol, DNP) or excised membrane patches (reduction of intracellular concentration of ATP as a common final pathway). DNP shortened the action potential
and
this
shortening resulted from an enhanced speed of repolarization of the plateau phase. Glibenclamide, a specific blocker of KATP channel. Prevented the DNP-induced shortening of the action potential and the DNP-induced single channel currents. The
KATP
channel activity was spontaneously active in the absence of ATP. It was closed by increasing [ATP]i. Glibenclamide (30 M) and various K+ channel blockers reversibly prevented channel opening. The [ATP]1 causing half-maximal inhibition of current
through
KATP channels (KA) was 70 M and Hill coefficient (n) was 1.2.
From the above results it could be suggested that the shortening of the action potential during metabolis inhibition is related to activation of KATP channels. Furthermore, opening or blocking the channel by therapeutic potential of K+ channel
modulators may be benificial or detrimental to the subsequent recovery of the heart after brief or prolonged periods of ischemia followed reperfusion, and modulation of KATP channel activity may be antiarrhythmic or arrhythmogenic primarily
depending on
the type of cardiac arrhythmia.
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KEYWORD
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