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目的探讨UⅡ(UrotensinⅡ)作用于大鼠心脏效应的电生理机制及可能的信号转导通路。方法利用全细胞膜片钳技术,给予不同浓度的UⅡ、KT5720+UⅡ及KT5720对照组后,观察大鼠心功能及心肌细胞L-型钙电流密度的变化。结果①运用全细胞膜片钳技术,在单个心肌细胞上给予不同浓度的UⅡ(10-9～10-5mol/L)灌流,Ica-L峰值分别下降为(6.70±1.78)pA/pF、(5.93±2.02)pA/pF、(5.40±2.15)pA/pF、(4.54±2.00)pA/pF、(3.80±1.82)pA/pF,与对照组(8.03±1.20)pA/pF相比,差异有统计学意义(P<0.05)。②在灌流KT5720的基础上给予UⅡ(IC50),Ica-L峰值二者比较变化不明显。结论 UⅡ呈浓度依赖性的抑制大鼠心肌细胞L-型钙电流强度,KT-5720可阻断UⅡ对大鼠心肌细胞钙电流的抑制作用,UⅡ可能通过PKA途径抑制心肌细胞L-型钙电流而发挥其心功能抑制作用。
Objective To investigate the electrophysiological mechanism and possible signal transduction pathways of U (Urotensin Ⅱ) in rat heart. Methods Whole-cell patch-clamp technique was used to observe the changes of cardiac function and L-type calcium current density in cardiomyocytes after different concentrations of UⅡ, KT5720 + UⅡ and KT5720 control group. Results ① Whole cell patch clamp technique was used to perfuse different concentrations of UⅡ (10-9 ~ 10-5mol / L) in single cardiomyocytes, the Ica-L peak decreased to (6.70 ± 1.78) pA / pF, PA / pF, (4.54 ± 2.00) pA / pF, (3.80 ± 1.82) pA / pF, respectively. Compared with the control group (8.03 ± 1.20) pA / pF, Statistical significance (P <0.05). ② The perfusion of KT5720 based on the given U Ⅱ (IC50), Ica-L peak of the two changes were not obvious. CONCLUSION: UⅡ can inhibit the L-type calcium current in rat cardiomyocytes in a concentration-dependent manner. KT-5720 can block the inhibitory effect of UⅡ on the calcium current in rat cardiomyocytes. UⅡ may inhibit the L-type calcium current in cardiomyocytes via PKA pathway And play its cardiac function inhibition.