HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/6/H3372    most recent 00997.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Isbell, D. C. Articles by Kramer, C. M. Search for Related Content PubMed PubMed Citation Articles by Isbell, D. C. Articles by Kramer, C. M.

Interaction between bradykinin subtype 2 and angiotensin II type 2 receptors during post-MI left ventricular remodeling

¹Cardiovascular Division, Department of Medicine, ²Department of Radiology, ³Department of Biomedical Engineering, and ⁴Department of Public Health Sciences, University of Virginia Health System, Charlottesville, Virginia; ⁵Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama; and ⁶Department of Cardiovascular Medicine, Kyoto Prefectural University School of Medicine, Kyoto, Japan

Submitted 29 August 2007 ; accepted in final form 5 October 2007

Angiotensin II type 2 receptor (AT₂R) overexpression (AT₂TG) attenuates left ventricular remodeling in a mouse model of anterior myocardial infarction (MI). We hypothesized that the beneficial effects of cardiac AT₂TG are mediated via the bradykinin subtype 2 receptor (B₂R). Fourteen transgenic mice overexpressing the AT₂R (AT₂TG mice), 10 mice with a B₂R deletion (B₂KO mice), 13 AT₂TG mice with B₂R deletion (AT₂TG/B₂KO mice), and 11 wild-type (WT) mice were studied. All mice were on a C57BL/6 background. Mice were studied by cardiac magnetic resonance imaging at baseline and days 1, 7, and 28 after MI induced by 1 h of occlusion of the left anterior descending artery followed by reperfusion. Short-axis images from apex to base were used to compare ventricular volumes and ejection fraction (EF). At baseline, end-diastolic volume index (EDVI) and end-systolic volume index (ESVI) were lower and EF higher in AT₂TG mice compared with the other three strains. Infarct size was similar between groups. No differences were observed in global remodeling parameters at day 28 between AT₂TG and AT₂TG/B₂KO mice; however, EDVI and ESVI were lower and EF higher in both transgenic groups than in WT or B₂KO mice. Both strains lacking B₂R demonstrated increased collagen content and less hypertrophy in adjacent noninfarcted regions at day 28. Attenuation of postinfarct remodeling by overexpression of AT₂R is not directly mediated via a B₂R pathway. However, B₂R does appear to have a role in the smaller cavity size and hyperdynamic function observed at baseline in AT₂TG mice and in limiting collagen deposition during postinfarct remodeling.

magnetic resonance imaging; remodeling