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Effects of des-aspartate-angiotensin I on neointima growth and cardiovascular hypertrophy

Sim Meng Kwoon1, Tang Feng Ru, Xu Xiao Guang

  • 1Department of Pharmacology, Faculty of Medicine, National University of Singapore, Building MD2, 18 Medical Drive, 117597, Singapore. phcsimmk@nus.edu.sg

Regulatory Peptides
|January 30, 2004
PubMed

Insights

Des-aspartate-angiotensin I (DAA-I) reduces neointima growth after arterial injury and prevents cardiac and vascular hypertrophy in hypertensive rats. These findings suggest DAA-I

Area of Science:

  • Cardiovascular Research
  • Endocrinology
  • Pharmacology

Background:

  • In vitro studies demonstrated des-aspartate-angiotensin I (DAA-I) possesses anti-hypertrophic and anti-hyperplastic effects on cardiovascular cells.
  • The role of endogenous angiotensins beyond angiotensin II in cardiovascular regulation requires further elucidation.

Purpose of the Study:

  • To investigate the in vivo effects of DAA-I on neointima formation following balloon catheter injury in rat carotid arteries.
  • To evaluate the impact of chronic DAA-I administration on cardiac and vascular hypertrophy in spontaneously hypertensive rats (SHR).

Main Methods:

  • Rats underwent balloon catheter injury to the carotid artery, followed by intravenous DAA-I treatment.
  • Pre-hypertensive SHR were orally administered DAA-I for 47 weeks.
  • Neointima area and cardiac/vascular hypertrophy were assessed and compared to control groups.

Main Results:

  • Intravenous DAA-I administration dose-dependently attenuated neointima development post-injury, with maximal efficacy at 34 pmol/kg/day.
  • Oral DAA-I treatment in SHR significantly reduced cardiac and vascular hypertrophy compared to untreated controls.
  • DAA-I had no observed effect on Wistar Kyoto rats, indicating specificity.

Conclusions:

  • Endogenous angiotensins, including DAA-I, may play a role in inhibiting neointima growth and cardiovascular hypertrophy.
  • DAA-I demonstrates therapeutic potential for conditions like restenosis and hypertension-induced cardiac remodeling.
  • These findings expand the understanding of angiotensin's involvement in cardiovascular pathophysiology.

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