Myocardial infarction initiates complex remodeling processes involving the renin–angiotensin system, through activation of the angiotensin II type 1 receptor (AT1R). This study correlated AT1R expression with fibrosis and cardiac function in the heart and kidneys following cardiac ischemic injury in animal models. Male Sprague-Dawley rats underwent Sham surgery, Ischemia/Reperfusion (I/R, 20-min ligation) or Permanent Ligation (PL) of the left anterior descending artery. Cardiac function was assessed by echocardiography. AT1R expression was measured in the heart (infarct and remote areas) and kidneys (cortex, medulla) via 125IodineSarcosine1-Isoleucine8-Angiotensin II autoradiography. Collagen deposition was evaluated through picrosirius red staining. Left ventricular (LV) ejection fraction declined in PL models but remained stable following I/R. Post-I/R, a transient increase in cardiac AT1R (day-3 to week-5) correlated with an increase in collagen, whereas after PL, elevations persisted through week-12. Infarct areas consistently displayed higher AT1R and collagen than remote areas. Renal AT1R and collagen levels were unchanged across groups. In analyses with pooled animals, cardiac AT1R expression correlated with collagen and inversely correlated with LV Fractional Shortening (LVFS), whereas LVFS inversely correlated with collagen deposition. These findings suggest that cardiac AT1R levels may serve as a target of cardiac remodeling, while changes in renal AT1R appear less pronounced.
Drumeva et al. (Wed,) studied this question.
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