Expression and localization of renin and angiotensinogen in the rat
heart following myocardial infarction.
Passier, Robert C. J. J., Jos F. M. Smits, Monique J. A. Verluyten,
and Mat J. A. P. Daemen.
University of Limburg, Cardiovascular Research Institute
Maastricht, Departments of Pharmacology and Pathology, Maastricht,
The Netherlands
APStracts 3:0128H, 1996.
Wistar Kyoto (WKY) rats underwent myocardial infarction (MI) or sham
-surgery. At different time points after surgery (1 to 90 days),
hearts were removed and divided into infarcted left ventricle (LV),
non-infarcted septum (SE) and right ventricle (RV). The tissues were
used for total RNA isolation or formalin fixation for in situ
hybridization (ISH). Renin and angiotensinogen mRNA contents were
quantified by the competitive reverse transcriptase polymerase chain
reaction. We found a 4, 14 and 8-fold increase (p<0.05; n=6) in
renin mRNA in the infarcted LV at 2, 4 and 7 days after MI,
respectively. No differences were observed between angiotensinogen
mRNA levels in sham and infarcted hearts. ISH at 4 days after
surgery, revealed a dense renin mRNA labeling around the infarcted
area, whereas ISH of angiotensinogen displayed an overall low density
in the myocardium with somewhat higher levels in the epicardium of
both sham and infarct animals. ANF mRNA, a marker for cardiac
hypertrophy was approximately 2-fold higher in all compartments of
the hearts after MI. The low amounts of renin and angiotensinogen
mRNA in the non-infarcted hypertrophied myocardium, indicate that the
intracardiac synthesis of these components does not play a dominant
role in the development of cardiac hypertrophy in the rat heart after
MI. In addition, the increased renin mRNA expression in the border
zone of the infarcted LV suggests a role for intracardiac angiotensin
II in infarct healing.
Received 5 September 1995; accepted in final form 26 February
1996.
APS Manuscript Number H833-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 April 96