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Basic science: Cardiovascular disease basic research
e0128 Angiotensin-(1-7) inhibits vascular remodelling in rat jugular vein grafts via reduced ERK1/2 and p38 MAPK activity
  1. Wu Jingguo1,
  2. Liang Yanbing1,
  3. Tang Hao1,
  4. Tang Anli2,
  5. Ma Zhongfu1,
  6. Ma Hong1
  1. 1The First Affiliated Hospital Sun Yat-sen University/Department of General Internal Medicine, Guangzhou, China
  2. 2The First Affiliated Hospital Sun Yat-sen University, Department of Cardiology, Guangzhou, China


Objects To evaluate the effects of Ang-(1-7) on vascular remodelling in vein grafts.

Methods a model of autologous jugular vein grafts in rats was established. With this model system, rats (n=12 per group) underwent autologous jugular vein graft transplantation (Ang-(1-7) and control groups), or a sham operation (sham group) in which grafting was not performed. Three days after operation, minipumps were installed for continuous infusion of Ang-(1-7) (25 μg/kg/h) or normal saline (control and sham groups) through the jugular vein.

Results 4 weeks, weight, blood pressure and heart rate were not significantly different between groups. Typical venous-graft hyperplasia, vascular remodelling, ERK1/2 activity, p38 MAPK activity and proliferating cell nuclear antigen (PCNA) and a-smooth muscle actin (a-SMA) expression present in the control group were attenuated by continuous Ang-(1-7) infusion. Tissue angiotensin II expression was increased in the Ang-(1-7) and control groups but was not different between the groups.

Conclusion The results of the present study indicate that exogenous Ang-(1-7) interferes with the vascular remodelling of autologous jugular vein grafts and significantly inhibits vein-graft intimal hyperplasia via inhibition of vascular tissue ERK1/2 and p38 MAPK activation. Thus, exogenous Ang-(1-7) improves the outcome of vein grafting via attenuation of vascular remodelling.

  • Ang-(1-7)
  • angiotensin
  • coronary artery bypass graft
  • vascular remodelling

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