摘要
目的 研究血管紧张素Ⅱ受体拮抗剂 (AngⅡ Antipeptide)对单个豚鼠心室肌细胞膜上L型钙通道电流 (ICa L)、ATP敏感钾通道电流 (IK ATP)延迟整流钾通道电流 (IK)、瞬间内向电流 (Iti)及内向整流钾通道电流 (IK1)的影响。方法 应用膜片钳全细胞记录方法。结果 (1)AngⅡ Antipeptide (5μmol/L)抑制ICa L,但并不改变I V曲线形态 ,(2 )AngⅡ Antipeptide (5 μmol/L)抑制IK ATP,(3 )AngⅡ Antipeptide (5 μmol/L)对IK 及IK·tail均有抑制作用 ,(4)AngⅡ Antipeptide (5 μmol/L)在低钾、高钙溶液中 ,抑制Iti电流 ,并明显延长滞后时间 (lag time) ,(5 )AngⅡ Antipeptide对内向整流钾通道电流 (Ik1)无明显作用。结论 AngⅡ Antipeptide对上述通道选择性不高 ,但推测它对以上通道综合影响在保护心肌及抗心律失常方面具有协同作用。
Objective To investigate the effects of angiontensin II receptor antipeptide (AngII antipeptide) on I K(ATP) , I Ca L , I K and I ti of guinea pig ventricular myocytes. Method Whole cell patch clamp technique was used. Results (1) I Ca L was inhibited by AngII antipeptide (5 μmol/L) (from -0 75±0 16 to -0 42± 0 09 nA, n =10, P< 0 05), but the shape of I V curve was not changed. (2) I K(ATP) was inhibited by AngII antipeptide (5 μmol/L) (1 52±0 24 to 0 94±0 13 nA, n =10, P < 0 05). (3) Both I K and I K·tail were inhibited by AngII antipeptide (5 μmol/L) (0 96±0 10 and 0 45± 0 08 nA to 0 40±0 06 and 0 18±0 06 nA, n = 8, P< 0 05, respectively). (4) In low K + high Ca 2+ solution, I ti was inhibited by AngII antipeptide (5 μmol/L) (-0 41±0 11 to -0 19±0 06 nA, n = 9, P< 0 05), and I ti lag time was significantly prolonged from 165±23 to 204±25 ms ( n = 9, P< 0 05). (5) AngII antipeptide (5 μmol/L) had no effects on I K1 . Conclusion AngII antipeptide might protect the ischemic cardiomyocytes and prevent arrhythmia.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2000年第1期58-60,共3页
Chinese Journal of Cardiology
关键词
血管紧张素Ⅱ
受体拮抗剂
心肌细胞
离子通道
Angiotensin Ⅱ antipeptide
Myocardium
Cells
Patch clamp techniques
Ion channels
