【摘要】 目的探讨内源性缓激肽对血管紧张素Ⅰ(AngⅠ)诱导乳鼠心肌细胞肥大的作用。方法体外原代培养新生Wistar大鼠的心肌细胞,随机分为对照组、AngⅠ组(10-9～10-5mol/L)、AngⅠ(10-6mol/L)+氯沙坦(losartan,Los)组、AngⅠ+卡托普利(captopril,Capt)组、AngⅠ+Capt+缓激肽B2受体拮抗剂(Hoe-140)组和AngⅠ+Capt+左旋硝基精氨酸(L-NNA)组,测量心肌细胞3H-亮氨酸掺入量、蛋白含量、细胞体积和搏动频率。结果 (1)AngⅠ可使培养的心肌细胞肥大,其作用有剂量依赖性。AngⅠ(10-6mol/L)引起心肌细胞肥大的作用与AngⅡ(10-7mol/L)相似;(2)Los可抑制AngⅠ的促肥大作用,与AngⅠ组相比,Los能使诱导3H-亮氨酸掺入量、总蛋白、细胞体积和搏动频率分别减少18.83%、18.66%、27.18%和26.37%(P<0.05);(3)Capt可抑制AngⅠ引起的心肌细胞肥大,其作用可被Hoe-140和L-NNA完全抑制。结论培养的心肌细胞可以将AngⅠ转化成AngⅡ,后者可使心肌细胞蛋白质合成增加、细胞体积增大,Capt通过减少AngⅡ生成和减少缓激肽降解抑制心肌细胞肥大。更多还原

【Abstract】 Objective To investigate the effect of endogenous bradykinin(BK)on hypertrophy of neonatal rat cardiomyocytes induced by angiotensinⅠ(AngⅠ).Methods Cardiomyocytes of neonatal Wistar rats were primarily cultured in vitro.The cardiomyocytes were randomly divided into control group,AngⅠ group(10-9-10-5 mol/L),AngⅠ(10-6 mol/L)+losartan group,AngⅠ+captopril(Capt group)AngⅠ+Capt+a specific BK2 receptor antagonist(Hoe-140)group and AngⅠ+Capt+L-NNA(an inhibitor of NOS)group,incorporation of 3H-Leu,total protein content,cellular volume,pulsatile frequency were observed.ResultsAngⅠ dose-dependently induced hypertrophy of cultured neonatal rat cardiomyocytes in serum-free medium.There is resemblance between the AngⅠ(10-6 mol/L)induced hypertrophy of cultured neonatal rat cardiomyocytes and Ang Ⅱ(10-7 mol/L);Losartan could inhibit the effect of AngⅠ on hypertrophy of cultured neonatal rat cardiomyocytes.Compared with the AngⅠ(5 d)group,the incorporation of 3H-Leu,total protein content,cellular volume,pulsatile frequency were decreased to 18.63%,18.86%,27.18% and 26.37% respectively(P<0.05);Captopril could inhibit the effect of AngⅠ on hypertrophy of cultured neonatal rat cardiomyocytes,this inhibitory effects were completely blocked by pretreatment with HOE-140,nitro-L-arginine(L-NNA).Conclusions AngⅠ can transform Ang II which shows that it exists ACE in cultured neonatal rat cardiomyocytes.AngⅠ can increase the total protein content and cellular volume,the effects of ACEI are due to both blockade of Ang II formation and inhibition of BK degradation.更多还原