From the Department of Medicine III (K.H., I.K., D.H., Y.Y.), University
of Tokyo School of Medicine, Tokyo, Japan; Lead Generation Research
Laboratories (T.S.), Tanabe Seiyaku Co, Ltd, Osaka, Japan; and Institute of
Applied Biochemistry (K.M.), University of Tsukuba, Ibaraki, Japan.
Correspondence to Issei Komuro, MD, Department of Medicine III, University of Tokyo School of Medicine, 7–3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan. E-mail komuro-tky{at}umin.u-tokyo.ac.jp
Background—A growing body of
evidence has suggested that the renin-angiotensin system
plays an important role in the development of cardiac
hypertrophy induced by hemodynamic overload
and left ventricular remodeling after myocardial
infarction. The role of the renin-angiotensin system in
ischemia-reperfusion (IR) injury, however, has not been
established.
Methods and Results—To determine the role of
angiotensin II (Ang II) in IR injury, we examined infarct
size and arrhythmias after IR using Ang II type 1a receptor
(AT1a) knockout mice. The left coronary artery was occluded for
30 minutes followed by reperfusion for 120 minutes. There were no
significant differences in infarct size between wild-type and knockout
mice determined by dual staining with
triphenyltetrazolium chloride and Evans
blue dye. The number of ventricular premature beats after
reperfusion in knockout mice, however, was much less than in wild-type
mice. Treatment with a selective AT1 antagonist, CV-11974,
before ischemia blocked reperfusion arrhythmias in
wild-type mice but had no effects on infarct size.
Conclusions—Ang II may be critically involved in the induction of
ventricular arrhythmias but not in the
determination of infarct size after IR.
© 1998 American Heart Association, Inc.
Brief Rapid Communications
Angiotensin II Type 1a Receptor Is Involved in the Occurrence of Reperfusion Arrhythmias
Key Words: reperfusion • arrhythmia • angiotensin • myocardial infarction
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