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. Author manuscript; available in PMC: 2021 Nov 25.
Published in final edited form as: Basic Res Cardiol. 2020 Nov 25;115(6):71. doi: 10.1007/s00395-020-00834-8

Fig. 1.

Fig. 1

Acute hyperglycemia regulates K+ channels in mouse ventricular cardiomyocytes. a Representative voltage-gated K+ current traces in normoglycemia and acute hyperglycemia. The transient outward K+ current (Ito) and slowly-inactivating K+ current (IK,slow) were inhibited by 3 mmol/L 4-aminopyiridine. Inset shows enlarged Ito. The steady-state K+ current (ISS) was insensitive to 4-aminopyridine. b Representative inward rectifier K+ current (IK1) traces. c Ito was significantly reduced in acute hyperglycemia. d, e IK,slow and ISS were unaltered in acute hyperglycemia. f Ito fast and slow inactivation time constants (τfast and τslow) were unchanged in acute hyperglycemia. g Ito recovery from inactivation was faster in hyperglycemia. h IK1 increased in acute hyperglycemia. Student’s paired t test, *p < 0.05, **p < 0.01, ***p < 0.001