1997
DOI: 10.1590/s0100-879x1997000500018
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Abstract: An increase in angiotensin-converting enzyme (ACE) activity has been observed in the heart after myocardial infarction (MI). Since most studies have been conducted in chronically infarcted individuals exhibiting variable degrees of heart failure, the present study was designed to determine ACE activity in an earlier phase of MI, before heart failure development. MI was produced in 3-month old male Wistar rats by ligation of the anterior branches of the left coronary artery, control rats underwent sham surgery … Show more

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Cited by 18 publications
(62 citation statements)
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References 31 publications
(62 reference statements)
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“…Several studies have reported increased expression of ACE in animal models of cardiac disease. ACE mRNA (24), enzyme activity (25), and protein levels identified by 125 I-MK351A (26) are demonstrated to increase in the left ventricle of rats after myocardial infarction induced by coronary artery ligation. The increase in ACE was predominantly in the border zone and scar tissue (24,25).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Several studies have reported increased expression of ACE in animal models of cardiac disease. ACE mRNA (24), enzyme activity (25), and protein levels identified by 125 I-MK351A (26) are demonstrated to increase in the left ventricle of rats after myocardial infarction induced by coronary artery ligation. The increase in ACE was predominantly in the border zone and scar tissue (24,25).…”
Section: Discussionmentioning
confidence: 99%
“…ACE mRNA (24), enzyme activity (25), and protein levels identified by 125 I-MK351A (26) are demonstrated to increase in the left ventricle of rats after myocardial infarction induced by coronary artery ligation. The increase in ACE was predominantly in the border zone and scar tissue (24,25). In addition, ACE mRNA increases in the left ventricle of senescent rats, which is suggested to be triggered by agerelated mechanical changes to the heart (27).…”
Section: Discussionmentioning
confidence: 99%
“…The cardiac RAAS is activated under several pathophysiological conditions, including MI and HF of different etiologies (27,28). Angiotensinogen is produced in infarcted hearts mainly by macrophages and fibroblasts, and ACE is extensively synthesized in endothelial cells and macrophages (29).…”
Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning
confidence: 99%
“…Angiotensinogen is produced in infarcted hearts mainly by macrophages and fibroblasts, and ACE is extensively synthesized in endothelial cells and macrophages (29). ACE activity increases in all regions of the infarcted heart, particularly in the scar tissue, leading to high local Ang II concentrations (27,30). ACE inhibition in infarcted rats reduces mortality, attenuates reactive fibrosis and myocyte hypertrophy and prevents HF development (16,26,30,31).…”
Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning
confidence: 99%
“…In dogs, detailed analyses have revealed that the RAS existing in cardiac tissue has a crucial role in the development of hypertrophy [2]. Cardiac ACE plays a role not only in generating Ang II, which provokes cardiac hypertrophy and fibrosis through Ang II type 1 (AT1) receptor signaling [4,12,23], but also in increasing cardiac fibrosis by catalyzing the degradation of bradykinin into inactive metabolites [3,9,26,30]. Similarly, cardiac chymase plays a role not only in converting Ang I to Ang II [31], but also in promoting direct collagen production [28,29].…”
Section: Discussionmentioning
confidence: 99%