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目的 以往的研究表明血管紧张素Ⅱ (AngⅡ )对心室肌细胞L型钙流 (ICa,L)的影响及作用机制尚有争议。本文应用AngⅡ 1型受体 (AT1)阻滞剂Losartan和蛋白激酶C(PKC)抑制剂H 7来研究AngⅡ对单个豚鼠心室肌细胞ICa ,L的作用及机制。方法 应用膜片钳技术研究AngⅡ对单个豚鼠心室肌细胞ICa ,L影响的细胞机制。结果 结果表明 ,在膜片钳全细胞记录模式 ,AngⅡ刺激ICa ,L,呈浓度依赖性 ,最大作用浓度为 10 0nmol/L (n =9)。30nmol/L的AngⅡ使ICa ,L峰电流由 11 3± 0 6pA/pF增大为 15 3± 0 6pA/pF( +10mV ,n =9,P <0 0 5)。 10 0nmol/L的Losartan本身对ICa ,L无影响 ,但可抑制AngⅡ对ICa,L的作用。AngⅡ对ICa,L的作用也能被 2 0nmol/L的H 7所抑制 ,而H 7本身对ICa,L无影响。结论 以上结果提示AngⅡ经AngⅡ 1型受体刺激ICa,L,这一作用经由PKC介导而实现。
Purpose Previous studies showed that the effect of angiotensin Ⅱ on L-type calcium current (ICa, L) in ventricular myocytes and its mechanism of action are controversial. In this paper, Losartan, an inhibitor of Ang II type 1 receptor (AT1), and H7, a protein kinase C (PKC) inhibitor, were used to study the effects of AngⅡ on ICa and L in isolated guinea pig ventricular myocytes. Methods Patch-clamp technique was used to study the cellular mechanism of AngⅡ on ICa, L of single guinea pig ventricular myocytes. The results showed that Ang Ⅱ stimulated ICa, L in a concentration-dependent manner in patch-clamp whole-cell recording mode with the maximum concentration of 10 nmol / L (n = 9). AngII at 30nmol / L increased the ICa, L peak current from 11 3 ± 0 6pA / pF to 15 3 ± 0 6pA / pF (+ 10mV, n = 9, P 0 05). 100 nmol / L of Losartan itself has no effect on ICa, L, but can inhibit Ang Ⅱ on ICa, L effect. The effect of AngⅡ on ICa, L can also be inhibited by 20 nmol / L H 7, while H 7 itself has no effect on ICa, L. Conclusion The above results suggest that AngⅡ is stimulated by AngⅡ type 1 receptor to ICa, L and this effect is mediated by PKC.