Inhibition of angiotensin-converting enzyme and attenuation of myocardial fibrosis by lisinopril in rats receiving angiotensin II.

Yao Sun, A. Ratajska, Karl Weber

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

High-density angiotensin-converting enzyme (ACE) binding is present in heart valve leaflets and the fibrous tissue that appears in the rat myocardium after either chronic administration of angiotensin II (AngII) or after myocardial infarction. This suggests that connective tissue ACE is independent of circulating AngII and that ACE may be an integral component of normal and pathologic tissue repair. To address this possibility the present study was undertaken. We sought to determine whether the ACE inhibitor lisinopril would attenuate fibrous tissue ACE binding and fibrous tissue formation in the myocardium of rats receiving AngII. Three experimental groups were examined: untreated, age-matched controls; rats receiving subcutaneous AngII (150 ng/min) by minipump for 2 weeks; and rats receiving AngII plus oral lisinopril (20 mg/kg/day) for 2 weeks. Cardiac ACE binding density was localized and quantified by in vitro autoradiography with [125I]-labeled 351A, a tyrosyl derivative of lisinopril, while fibrosis was identified by light microscopy in serial sections stained with picrosirius red. Hematoxylin and eosin and anti-fibronectin antibody were used to identify cardiac myocyte necrosis. Immunohistochemical labeling with alpha-smooth muscle actin was used to identify myofibroblasts.(ABSTRACT TRUNCATED AT 250 WORDS)

Original languageEnglish (US)
Pages (from-to)95-101
Number of pages7
JournalJournal of Laboratory and Clinical Medicine
Volume126
Issue number1
StatePublished - Jul 1995
Externally publishedYes

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Lisinopril
Peptidyl-Dipeptidase A
Angiotensin II
Rats
Fibrosis
Tissue
Myocardium
Myofibroblasts
Heart Valves
Hematoxylin
Eosine Yellowish-(YS)
Autoradiography
Fibronectins
Angiotensin-Converting Enzyme Inhibitors
Cardiac Myocytes
Connective Tissue
Labeling
Optical microscopy
Smooth Muscle
Muscle

All Science Journal Classification (ASJC) codes

  • Medicine(all)
  • Pathology and Forensic Medicine

Cite this

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title = "Inhibition of angiotensin-converting enzyme and attenuation of myocardial fibrosis by lisinopril in rats receiving angiotensin II.",
abstract = "High-density angiotensin-converting enzyme (ACE) binding is present in heart valve leaflets and the fibrous tissue that appears in the rat myocardium after either chronic administration of angiotensin II (AngII) or after myocardial infarction. This suggests that connective tissue ACE is independent of circulating AngII and that ACE may be an integral component of normal and pathologic tissue repair. To address this possibility the present study was undertaken. We sought to determine whether the ACE inhibitor lisinopril would attenuate fibrous tissue ACE binding and fibrous tissue formation in the myocardium of rats receiving AngII. Three experimental groups were examined: untreated, age-matched controls; rats receiving subcutaneous AngII (150 ng/min) by minipump for 2 weeks; and rats receiving AngII plus oral lisinopril (20 mg/kg/day) for 2 weeks. Cardiac ACE binding density was localized and quantified by in vitro autoradiography with [125I]-labeled 351A, a tyrosyl derivative of lisinopril, while fibrosis was identified by light microscopy in serial sections stained with picrosirius red. Hematoxylin and eosin and anti-fibronectin antibody were used to identify cardiac myocyte necrosis. Immunohistochemical labeling with alpha-smooth muscle actin was used to identify myofibroblasts.(ABSTRACT TRUNCATED AT 250 WORDS)",
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AU - Sun, Yao

AU - Ratajska, A.

AU - Weber, Karl

PY - 1995/7

Y1 - 1995/7

N2 - High-density angiotensin-converting enzyme (ACE) binding is present in heart valve leaflets and the fibrous tissue that appears in the rat myocardium after either chronic administration of angiotensin II (AngII) or after myocardial infarction. This suggests that connective tissue ACE is independent of circulating AngII and that ACE may be an integral component of normal and pathologic tissue repair. To address this possibility the present study was undertaken. We sought to determine whether the ACE inhibitor lisinopril would attenuate fibrous tissue ACE binding and fibrous tissue formation in the myocardium of rats receiving AngII. Three experimental groups were examined: untreated, age-matched controls; rats receiving subcutaneous AngII (150 ng/min) by minipump for 2 weeks; and rats receiving AngII plus oral lisinopril (20 mg/kg/day) for 2 weeks. Cardiac ACE binding density was localized and quantified by in vitro autoradiography with [125I]-labeled 351A, a tyrosyl derivative of lisinopril, while fibrosis was identified by light microscopy in serial sections stained with picrosirius red. Hematoxylin and eosin and anti-fibronectin antibody were used to identify cardiac myocyte necrosis. Immunohistochemical labeling with alpha-smooth muscle actin was used to identify myofibroblasts.(ABSTRACT TRUNCATED AT 250 WORDS)

AB - High-density angiotensin-converting enzyme (ACE) binding is present in heart valve leaflets and the fibrous tissue that appears in the rat myocardium after either chronic administration of angiotensin II (AngII) or after myocardial infarction. This suggests that connective tissue ACE is independent of circulating AngII and that ACE may be an integral component of normal and pathologic tissue repair. To address this possibility the present study was undertaken. We sought to determine whether the ACE inhibitor lisinopril would attenuate fibrous tissue ACE binding and fibrous tissue formation in the myocardium of rats receiving AngII. Three experimental groups were examined: untreated, age-matched controls; rats receiving subcutaneous AngII (150 ng/min) by minipump for 2 weeks; and rats receiving AngII plus oral lisinopril (20 mg/kg/day) for 2 weeks. Cardiac ACE binding density was localized and quantified by in vitro autoradiography with [125I]-labeled 351A, a tyrosyl derivative of lisinopril, while fibrosis was identified by light microscopy in serial sections stained with picrosirius red. Hematoxylin and eosin and anti-fibronectin antibody were used to identify cardiac myocyte necrosis. Immunohistochemical labeling with alpha-smooth muscle actin was used to identify myofibroblasts.(ABSTRACT TRUNCATED AT 250 WORDS)

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