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目的:观察胍丁胺(Agm)对大鼠心室肌细胞L-型钙通道电流(I_(Ca-L))的影响.方法:以酶解法制备单个心室肌细胞.应用全细胞膜片箝技术记录大鼠单个心室肌细胞钙通道电流.结果:(1)Agm(0.5,1,2mmol/L)可浓度依赖性地降低电压依赖性激活I_(Ca-L)(pA)峰值,其值从1451±236 (对照组)到937±105(n=8,P<0.05),585±74(n=8,P<0.01),和301±156(n=8,P<0.01).(2)Agm 1 mmol/L使用依赖性地阻滞I_(Ca-L)·1 Hz时抑制率为53％±12％(P<0.05),3Hz时为69％±11％(P<0.01).(3)Agm使I-V曲线上移,但对I_(Ca-L)的电压依赖特征、最大激活电压以及I_(Ca-L)稳态激活无明显影响.在Agm 1 mmol/L作用下,半数激活电压(V_(0.5)和斜率参数(k)与对照组相比均无显著性差异.V_(0.5)分别为(-20.2±2.5)mV和(-20.5±2.7)mV,k分别为(3.2±0.4)mV和(3.0±0.5)mV.(4)Agm 1 mmol/L可明显使钙电流稳态失活曲线左移,加速钙通道电压依赖性稳态失活.V_(0.5)分别为(-32±6)mV和(-40±5)mV,k分别为(7.6±O.9)mV和(12.5±1.1)mV(P<0.05).(5)Agm 1mmol/L还使I_(Ca)从失活状态下恢复明显减慢.结论:Agm抑制I_(Ca-L),并主要作用于L-型钙通道的失活状态,表现为钙通道失活加速和从失活状态下恢复减慢.
OBJECTIVE: To observe the effect of agmatine on L-type calcium channel current (I_ (Ca_ L)) in rat ventricular myocytes.Methods: Single ventricular myocytes were prepared by enzymolysis method and recorded using whole-cell patch clamp technique (1) Agm (0.5,1,2mmol / L) could decrease the peak of voltage-dependent activation I_ (Ca-L) (pA) in a concentration-dependent manner, from 1451 (Control group) to 937 ± 105 (n = 8, P <0.05), 585 ± 74 (n = 8, P <0.01) and 301 ± 156 (n = 8, The inhibitory rate of 1 mmol / L Agm was 53% ± 12% (P <0.05) at 1 Hz and 69% ± 11% at 3 Hz (P <0.01). 3) Agm up-regulated the IV curve, but had no significant effect on the voltage-dependent characteristics of I_ (Ca-L), maximum activation voltage and I_ (Ca-L) There was no significant difference between voltage (V_ (0.5) and slope parameter (k)) and control group (V_ (0.5) were respectively -20.2 ± 2.5 mV and -20.5 ± 2.7 mV, ± 0.4) mV and (3.0 ± 0.5) mV. (4) Agm 1 mmol / L could obviously shift the steady-state inactivation curve of calcium current to the left and accelerate the voltage-dependent steady state inactivation of calcium channels. (-32 ± 6) mV and (-40 ± 5) mV, k, respectively (7.6 ± 0.9) mV and (12.5 ± 1.1) mV respectively (P <0.05). (5) Agm 1mmol / L also slowed the recovery of I_ (Ca) from inactivation state.Conclusion: Agm inhibits I_ ( Ca-L), and mainly acts on the inactivation state of L-type calcium channel, which is characterized by acceleration of calcium channel inactivation and recovery from inactivation state.