摘要
应用膜片钳全细胞记录技术研究血管紧张素 (1 7) [Ang (1 7) ]和血管紧张素 Ⅱ (AngⅡ )对豚鼠心室肌细胞钾离子通道作用的异同 ,并探讨Ang (1 7)发挥作用的机制。结果 :2 μmol/LAng (1 7)可使延迟整流性钾离子流 (Ik)从 13.5 3± 0 .92 pA/ pF增至 17.5 8± 2 .73pA/ pF(P <0 .0 5 ) ,应用选择性AT1受体拮抗剂缬沙坦 (Val)后 ,Ang (1 7)增加IK 的作用依然存在 ,而应用非选择性血管紧张素 (AT)受体拮抗剂Sarthran (Sar)后 ,Ang (1 7)对IK 的作用被消除。同样浓度的Ang (1 7)对内向整流性钾离子流 (IK1)无影响 (P >0 .0 5 )。 2 μmol/LAngⅡ可使Ik从13.94± 1.4 9pA/pF降至 8.98± 2 .4 6 pA/ pF(P <0 .0 1)、IK1的内向电流从 38.6 7± 8.2 4 pA/pF增至 5 3.4 7±7.4 8pA/pF(P <0 .0 1)。应用Val和Sar后 ,AngⅡ抑制IK 的作用被消除 ,而只有Sar可以消除AngⅡ增加IK1的作用。结论 :Ang (1 7)通过非AT1受体增加IK,对IK1无影响 ;AngⅡ通过AT1受体抑制IK,通过非AT1受体增加IK1,二者对钾离子流的作用不同。
To investigate the effects of Ang-(1-7) and AngⅡ on potassium channels in guinea pig myocytes. Potassium currents were recorded with patch electrodes in a whole-cell clamp configuration. Results:Ang-(1-7) 2μmol/L increased the amplitude of I_k from 13.53±0.92pA/pF to 17.58±2.73pA/pF( P <0.05). However,AngⅡ 2μmol/L decreased the amplitude of I_k from 13.94±1.49pA/pF to 8.96±2.46pA/pF( P <0.01). The effects of Ang-(1-7) or AngⅡ on I_k could be almost completely eliminated by Sarthran,but Valsartan could not. The amplitude of I_ K1 was not affected by Ang-(1-7) 2μmol/L( P >0.05) ,but was increased by AngⅡ 2μmol/L from -38.67±8.24pA/pF to -53.47±7.48pA/pF( P <0.01). Sarthran eliminated the effect of AngⅡ on I_ K1 ,but Valsarthan did not. Conclusions: Ang-(1-7) increases the amplitude of I_k through non specific AT_1 receptor. AngⅡ decreases the amplitude of I_k through specific AT_1 receptor. I_ K1 is increased by AngⅡ through non specific AT receptor.
出处
《中国心脏起搏与心电生理杂志》
2004年第1期52-56,共5页
Chinese Journal of Cardiac Pacing and Electrophysiology
