Egg-derived tri-peptide IRW exerts antihypertensive effects in spontaneously hypertensive rats

• Author(s) / Creator(s)

  • Majumder, Kaustav
  • Kaufman, Susan
  • Chakrabarti, Subhadeep
  • Morton, Jude S.
  • Panahi, Sareh
  • Wu, Jianping
  • Davidge, Sandra T.

• Background There is a growing interest in using functional food components as therapy for cardiovascular diseases such as hypertension. We have previously characterized a tri-peptide IRW (Ile-Arg-Trp) from egg white protein ovotransferrin; this peptide showed anti-inflammatory, anti-oxidant and angiotensin converting enzyme (ACE) inhibitor properties in vitro. Given the pathogenic roles played by angiotensin, oxidative stress and inflammation in the spontaneously hypertensive rat (SHR), we tested the therapeutic potential of IRW in this well-established model of hypertension. Methods and Results 16–17 week old male SHRs were orally administered IRW at either a low dose (3 mg/Kg BW) or a high dose (15 mg/Kg BW) daily for 18 days. Blood pressure (BP) and heart rate were measured by telemetry. Animals were sacrificed at the end of the treatment for vascular function studies and measuring markers of inflammation. IRW treatment attenuated mean BP by ~10 mmHg and ~40 mmHg at the low- and high-dose groups respectively compared to untreated SHRs. Heart rate was not affected. Reduction in BP was accompanied by the restoration of diurnal variations in BP, preservation of nitric oxide dependent vasorelaxation, as well as reduction of plasma angiotensin II, other inflammatory markers and tissue fibrosis. Conclusion Our results demonstrate anti-hypertensive effects of IRW in vivo likely mediated through ACE inhibition, endothelial nitric oxide synthase and anti-inflammatory properties.

• Date created

  2013

• Subjects / Keywords

  • Blood Pressure
  • Antioxidants
  • Nitric Oxide
  • Blood Plasma
  • Mesenteric Arteries
  • Hypertension
  • ACE Inhibitors
  • Inflammation

• Type of Item

  Article (Published)

• DOI

  https://doi.org/10.7939/R38W38G20

• License

  Attribution 4.0 International