Published online Feb 15, 2003. doi: 10.3748/wjg.v9.i2.329
Revised: October 4, 2002
Accepted: October 17, 2002
Published online: February 15, 2003
AIM: To study the effects of palmatine, a known inhibitor on delayed rectifier potassium current and L-type calcium current (ICa,L) in guinea pig ventricular myocytes, on the potassium and calcium currents in isolated rat hepatocytes.
METHODS: Tight-seal whole-cell patch-clamp techniques were performed to investigate the effects of palmatine on the delayed outward potassium currents (IK), inward rectifier potassium current (IK1) and Ca2+ release-activated Ca2+ current (ICRAC) in enzymatically isolated rat hepatocytes.
RESULTS: Palmatine 0.3-100 μM reduced IK in a concentration-dependent manner with EC50 of 41.62 ± 10.11 μM and nH, 0.48 ± 0.07 (n = 8). The effect of the drug was poorly reversible after washout. When the bath solution was changed to tetraethylammonium (TEA) 8 mM, IK was inhibited. Palmatine 10 μM and 100 μM shifted the I-V curves of IK downward, and the block of IK was voltage-independent. Palmatine 0.3-100 μM also inhibited ICRAC in a concentration-dependent manner. The fitting parameters were as follows: EC50 = 51.19 ± 15.18 mM, and nH = 0.46 ± 0.07 (n = 8). The peak value of ICRAC in the I-V relationship was decreased by palmatine 10 μM and 100 μM. But the reverse potential of ICRAC occurred at Voltage = 0 mV in all cells. Palmatine 0.3-100 μM failed to have any significant effect on either inward or outward components of IK1 at any membrane potential examined.
CONCLUSION: The inhibitory effects on IK and ICRAC could be one of the mechanisms that palmatine exerts protective effect on hepatocytes.