ABSTRACT
<p><b>AIM</b>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.</p><p><b>METHODS</b>The delayed rectifier potassium current was recorded by using whole cell arrangement of the patch-clamp procedure.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>Ik was increased by both PKA and PKC, with different characteristics of regulation.</p>
Subject(s)
Animals , Female , Male , Cyclic AMP-Dependent Protein Kinases , Pharmacology , Delayed Rectifier Potassium Channels , Metabolism , Guinea Pigs , Heart Ventricles , Cell Biology , Myocytes, Cardiac , Metabolism , Patch-Clamp Techniques , Potassium , Metabolism , Protein Kinase C , PharmacologyABSTRACT
<p><b>AIM</b>To investigate the effect of benzyltetrahydropalmatine (BTHP) on the rapidly activating component of delayed rectifier K+ current (Ikr) in single guinea pig ventricular myocytes.</p><p><b>METHODS</b>Whole-cell patch clamp technique was used to record Ikr.</p><p><b>RESULTS</b>Ikr was blocked by 1-100 mumol.L-1 BTHP in concentration-, voltage-, and specifically frequency-dependent fashion, with IC50 of 13.5 mumol.L-1 (95% confidence range: 11.2-15.8 mumol.L-1). 30 mumol.L-1 BTHP reduced Ikr and Ikr.tail by (31 +/- 4)% and (36 +/- 5)% (n = 6, P < 0.01), respectively. The time constant for deactivation (tau') of the tail current was decreased by 30 mumol.L-1 BTHP from (238 +/- 16) ms to (196 +/- 14) ms, while drug had no any effect on the time constant for activation (tau) of Ikr,tail.</p><p><b>CONCLUSION</b>BTHP inhibited Ikr in a frequency-dependent fashion.</p>