Direct Evidence for Increased Hydroxyl Radicals in Angiotensin II-induced Cardiac Hypertrophy through Angiotensin II Type 1a Receptor

Mikio Kakishita, Kazufumi Nakamura, Masato Asanuma, Hiroshi Morita, Hironori Saito, Kengo Kusano, Yoichi Nakamura, Tetsuro Emori, Hiromi Matsubara, Takeshi Sugaya, Norio Ogawa, Tohru Ohe

Research output: Contribution to journalArticlepeer-review

25 Citations (Scopus)

Abstract

Oxidative stress is known to contribute to numerous cardiac disease processes. However, the contribution of reactive oxygen species to cardiac hypertrophy has not yet been fully investigated. The aim of the present study was therefore to determine whether levels of reactive oxygen species were increased in angiotensin II-induced cardiac hypertrophy. We continuously administered angiotensin II (1.1 mg/kg per day) into wild-type and angiotensin II type-1a receptor knockout mice for 2 weeks. The angiotensin II treatment increased blood pressure and heart weight/body weight ratio in wild-type mice but not in knockout mice. The generation of hydroxyl radicals in heart tissue homogenate was directly assessed with electron spin resonance spectroscopy using a spin trapping agent, alpha-phenyl-N-tert butylnitrone. Angiotensin II significantly increased hydroxyl radical production 2.2-fold (p < 0.01) in the hearts of wild-type mice but not in knockout mice. The present study provided direct evidence for increased production of hydroxyl radicals in angiotensin II-induced cardiac hypertrophy through angiotensin II type-1 a receptor. These findings in this study may provide important insights into the development of hypertrophy and the transition of hypertrophy to heart failure.

Original languageEnglish
Pages (from-to)S67-S70
JournalJournal of cardiovascular pharmacology
Volume42
Issue numberSUPPL. 1
DOIs
Publication statusPublished - Dec 2003

Keywords

  • Angiotensin II
  • Angiotensin II type-1a receptor
  • Cardiac hypertrophy
  • Hydroxyl radical
  • Oxidative stress

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

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