Effects of low-dose capsaicin on L-type calcium current in guinea pig ventricular myocytes

The purpose of this study was to examine the effects of low-dose capsaicin (CAP) on L-type calcium current (ICu- L) in guinea pig ventricular myocytes and the underlying mechanism. ICa-L was examined in isolated single guinea pig ventricular myocytes by using whole-cell patch clamp technique. CAP (1-25 nmol/L) increased the voltage-dependently activated peak amplitude of ICa-L and downshifted the current-voltage (I-V) curve. CAP (1,10,25 nmol/L) increased the peak amplitude of ICa-L from -9.67±0.7 pA/pF to -10.21±0.8 pA/pF (P 0.05), to -11.37±?0.8 pA/pF and to -12.84±0.9 pA/pF (P0.05), respectively. CAP 25 nmol/L shifted the steady-state activation curve ofICa-Lto the left and changed half activation potential (V0.5) from (-20.76±2.0) mV to (-26.71±2.0) mV (P0.05), indicating that low-dose CAP may modify the voltage-dependent activation of calcium channel. Low-dose of CAP did not affect the steady-state inactivation curve of ICa-L or half-recovery time of Ca2+ channel from inactivation. Ruthenium red (RR, 10 μmol/L), a vanilloid receptor (VR1) blocker, antagonized the effects of low-dose CAP. These results suggest that low-dose CAP increases ICa-L mainly by shifting its steady-state activation curve to the left. Such effects may be mediated by VR1.