[Modulation of protein kinase A and protein kinase C on the delayed rectifier potassium current in guinea pig ventricular myocytes]
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Updated: Jun 5, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Yang Li1, Li-ying Fu, Wei-xing Yao
1Department of Cardiology, Tongji Hospital, China.
Aim:
To study modulation of protein kinase A (PKA) and protein kinase C (PKC) on the delayed rectifier potassium current (Ik)in guinea pig ventricular myocytes.
Methods:
The delayed rectifier potassium current was recorded by using whole cell arrangement of the patch-clamp procedure.
Results:
cAMP 150 micromol/L increased intracellularly Ik and Ik,tail(pA/pF) from 13.7 +/- 2.1 and 6.1 +/- 0.1 to 18.5 +/- 3.3 and 6.4 +/- 2.1 (P < 0.01, n=6). Ik and Ik,tail(pA/pF) were augmented by 8-CPT-cAMP 150 micromol/L extracellularly from 11.4 +/- 1.8 and 5.3 +/- 0.6 to 17.9 +/- 4.0 and 6.2 +/- 1.3. The half-maximal voltage of activation of Ik was shifted from + 23.3 mV to 18.7 mV by cAMP. Phorbol 12-myristate 13-acetate(PMA, 10.0 micromol/L) applied intracellularly caused an enhance effect on Ik, with increasing Ik and Ik,tail(pA/pF) from 12.9 +/- 1.8 and 5.0 +/- 1.7 to 23.7 +/- 2.8 and 7.5 +/- 1.1. With shifting position potential of depolarization, effect of PMA on Ik was gradually augmented. PMA resulted in shifting the slop of activation curve from +15.3 mV to +25.6 mV, with only a small effect on the half-maximal voltage of activation of Ik.
Conclusion:
Ik was increased by both PKA and PKC, with different characteristics of regulation.
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