Key result
Glibenclamide accelerated the inactivation time-course of the total outward current in human atrial myocytes, reducing tau(fast) from 12.7 to 5.8 ms (P<0.001).
Why the study?
Does glibenclamide inhibit voltage-dependent potassium currents in human atrial and ventricular myocytes?
Does glibenclamide inhibit voltage-dependent potassium currents in human atrial and ventricular myocytes?
Absolute Event Rate: 5.8% vs 12.7%
p-value: p=<0.001
Glibenclamide inhibits voltage-dependent cardiac potassium currents, specifically Ito1 and IKur, in human atrial and ventricular myocytes at concentrations above 10 microM.
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May alter atrial repolarization at high doses; hypothesis-generating for sulfonylurea effects on human cardiac K+ currents.
Schäffer et al. (1999) studied this question. Glibenclamide vs. Control was evaluated on tau(fast) of the total outward current inactivation time-course (p=<0.001). Glibenclamide accelerated the inactivation time-course of the total outward current in human atrial myocytes, reducing tau(fast) from 12.7 to 5.8 ms (P<0.001).
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