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应用全细胞膜片钳技术研究低浓度辣椒素(capsaicin,cAP)对单个豚鼠心室肌细胞L-型钙电流的影响及其作用机制。CAP(1-25 nmol/L)可浓度依赖性增加电压依赖性的ICa-L的峰值并下移I-V曲线。CAP 1,10,25 nmol/L使ICa-L最大峰值分别由-9.67±0.7pA/pF增至-10.21±0.8 pA/pF(P>0.05),-11.37±0.8 pA/pF和-12.84±0.9 pA/pt(P<0.05)。CAP 25 nmol/L可明显使稳态激活曲线左移,激活中点电压(V0.5)由-20.76±2.0mV变至-26.71±3.0mV(P<0.05),表明低浓度CAP改变了钙通道激活的电压依赖性。CAP25 nmol/L对电压依赖性稳态失活曲线和ICa-L从失活状态下复活过程无明显影响。辣椒素受体(VRl)阻断剂钌红(RR,10 μmol/L可阻断低浓度辣椒素的效应。以上结果表明,低浓度辣椒素使钙通道稳态激活曲线左移,增加ICa-L这一效应可能由VR1介导。
Whole-cell patch clamp technique was used to study the effect of capsaicin (cAP) on L-type calcium current in isolated guinea pig ventricular myocytes and its mechanism. CAP (1-25 nmol / L) increased the peak of voltage-dependent ICa-L in a concentration-dependent manner and shifted down the I-V curve. CAP 1, 10 and 25 nmol / L increased the maximum ICa-L peak from -9.67 ± 0.7pA / pF to -10.21 ± 0.8 pA / pF (P> 0.05), -11.37 ± 0.8 pA / pF and -12.84 ± 0.9 pA / pt (P <0.05). CAP 25 nmol / L could obviously shift the steady-state activation curve to the left, and the activation midpoint voltage (V0.5) changed from -20.76 ± 2.0 mV to -26.71 ± 3.0 mV (P <0.05), indicating that low concentration of CAP changed calcium Channel-dependent voltage dependence. No significant effect of CAP25 nmol / L on voltage-dependent steady-state inactivation curve and ICa-L resuscitation from inactivated state. The RR1 blocker ruthenium red (RR, 10 μmol / L can block the low concentration of capsaicin effect.The above results show that the low concentration of capsaicin calcium channel steady-state activation curve shifted to the left, increasing ICa- This effect of L may be mediated by VR1.