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Inhibition of angiotensin-converting enzyme and attenuation of myocardial fibrosis by lisinopril in rats receiving angiotensin II.
J Lab Clin Med. 1995 Jul; 126(1):95-101.JL

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)

Authors+Show Affiliations

Department of Internal Medicine, University of Missouri-Columbia 65212, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

7602241

Citation

Sun, Y, et al. "Inhibition of Angiotensin-converting Enzyme and Attenuation of Myocardial Fibrosis By Lisinopril in Rats Receiving Angiotensin II." The Journal of Laboratory and Clinical Medicine, vol. 126, no. 1, 1995, pp. 95-101.
Sun Y, Ratajska A, Weber KT. Inhibition of angiotensin-converting enzyme and attenuation of myocardial fibrosis by lisinopril in rats receiving angiotensin II. J Lab Clin Med. 1995;126(1):95-101.
Sun, Y., Ratajska, A., & Weber, K. T. (1995). Inhibition of angiotensin-converting enzyme and attenuation of myocardial fibrosis by lisinopril in rats receiving angiotensin II. The Journal of Laboratory and Clinical Medicine, 126(1), 95-101.
Sun Y, Ratajska A, Weber KT. Inhibition of Angiotensin-converting Enzyme and Attenuation of Myocardial Fibrosis By Lisinopril in Rats Receiving Angiotensin II. J Lab Clin Med. 1995;126(1):95-101. PubMed PMID: 7602241.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of angiotensin-converting enzyme and attenuation of myocardial fibrosis by lisinopril in rats receiving angiotensin II. AU - Sun,Y, AU - Ratajska,A, AU - Weber,K T, PY - 1995/7/1/pubmed PY - 1995/7/1/medline PY - 1995/7/1/entrez SP - 95 EP - 101 JF - The Journal of laboratory and clinical medicine JO - J Lab Clin Med VL - 126 IS - 1 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) SN - 0022-2143 UR - https://www.unboundmedicine.com/medline/citation/7602241/Inhibition_of_angiotensin_converting_enzyme_and_attenuation_of_myocardial_fibrosis_by_lisinopril_in_rats_receiving_angiotensin_II_ L2 - https://www.lens.org/lens/search/patent/list?q=citation_id:7602241 DB - PRIME DP - Unbound Medicine ER -