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Angiotensin II receptor binding following myocardial infarction in the rat.
Cardiovasc Res. 1994 Nov; 28(11):1623-8.CR

Abstract

OBJECTIVE

The aim was to determine angiotensin II receptor binding and its relationship to angiotensin converting enzyme (ACE) binding and fibrous tissue formation in the rat heart.

METHODS

A model of tissue repair (pericardiotomy and myocardial infarction with left coronary artery ligation) was used together with the following: quantitative in vitro autoradiography to determine angiotensin II receptor (125I[Sar1, Ile8]AngII) and ACE (125I-351A) binding densities. Angiotensin II receptor subtype was determined using an AT1 receptor antagonist (DuP753, losartan) and an AT2 receptor antagonist (PD123177). Five groups were studied: age and sex matched controls receiving this operative procedure without subsequent myocardial infarction (sham operated); rats with coronary artery ligation and myocardial infarction; rats with coronary artery ligation and lisinopril (20 mg.kg-1.d-1 in drinking water); sham operated rats receiving lisinopril; and unoperated rats which served as controls to pericardiotomy. Hearts were collected from each group on postoperative day 3 and weeks 1, 2, 4, and 8.

RESULTS

There was (1) low angiotensin receptor binding in normal myocardium; (2) markedly increased angiotensin II receptor binding at the site of left ventricular myocardial infarction and endocardial fibrosis of the interventricular septum at day 3 and weeks 1, 2, 4, and 8; (3) high angiotensin II receptor binding in the pericardial fibrosis that followed pericardiotomy, and in the fibrosis that appeared in response to suture insertion around the left coronary artery, in both infarcted and sham operated rats; (4) total displacement of normal and connective tissue angiotensin II receptor binding by DuP753, but not by PD123177; (5) ACE inhibition by lisinopril, but no change in angiotensin II receptor binding, at all sites of fibrosis; and (6) significant attenuation by lisinopril of collagen formation in the visceral pericardium of sham operated controls.

CONCLUSIONS

In this model of tissue repair, increased AT1 receptor binding density is associated with ACE binding and fibrillar collagen formation that appears within sites of fibrous tissue formation, including myocardial infarction, endocardial fibrosis, foreign body (silk suture), and pericardiotomy. AT1 receptors may play a role in mediating the fibrogenic response to tissue injury in the rat heart.

Authors+Show Affiliations

Division of Cardiology, University of Missouri-Columbia 65212.No affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

7842454

Citation

Sun, Y, and K T. Weber. "Angiotensin II Receptor Binding Following Myocardial Infarction in the Rat." Cardiovascular Research, vol. 28, no. 11, 1994, pp. 1623-8.
Sun Y, Weber KT. Angiotensin II receptor binding following myocardial infarction in the rat. Cardiovasc Res. 1994;28(11):1623-8.
Sun, Y., & Weber, K. T. (1994). Angiotensin II receptor binding following myocardial infarction in the rat. Cardiovascular Research, 28(11), 1623-8.
Sun Y, Weber KT. Angiotensin II Receptor Binding Following Myocardial Infarction in the Rat. Cardiovasc Res. 1994;28(11):1623-8. PubMed PMID: 7842454.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Angiotensin II receptor binding following myocardial infarction in the rat. AU - Sun,Y, AU - Weber,K T, PY - 1994/11/1/pubmed PY - 1994/11/1/medline PY - 1994/11/1/entrez SP - 1623 EP - 8 JF - Cardiovascular research JO - Cardiovasc Res VL - 28 IS - 11 N2 - OBJECTIVE: The aim was to determine angiotensin II receptor binding and its relationship to angiotensin converting enzyme (ACE) binding and fibrous tissue formation in the rat heart. METHODS: A model of tissue repair (pericardiotomy and myocardial infarction with left coronary artery ligation) was used together with the following: quantitative in vitro autoradiography to determine angiotensin II receptor (125I[Sar1, Ile8]AngII) and ACE (125I-351A) binding densities. Angiotensin II receptor subtype was determined using an AT1 receptor antagonist (DuP753, losartan) and an AT2 receptor antagonist (PD123177). Five groups were studied: age and sex matched controls receiving this operative procedure without subsequent myocardial infarction (sham operated); rats with coronary artery ligation and myocardial infarction; rats with coronary artery ligation and lisinopril (20 mg.kg-1.d-1 in drinking water); sham operated rats receiving lisinopril; and unoperated rats which served as controls to pericardiotomy. Hearts were collected from each group on postoperative day 3 and weeks 1, 2, 4, and 8. RESULTS: There was (1) low angiotensin receptor binding in normal myocardium; (2) markedly increased angiotensin II receptor binding at the site of left ventricular myocardial infarction and endocardial fibrosis of the interventricular septum at day 3 and weeks 1, 2, 4, and 8; (3) high angiotensin II receptor binding in the pericardial fibrosis that followed pericardiotomy, and in the fibrosis that appeared in response to suture insertion around the left coronary artery, in both infarcted and sham operated rats; (4) total displacement of normal and connective tissue angiotensin II receptor binding by DuP753, but not by PD123177; (5) ACE inhibition by lisinopril, but no change in angiotensin II receptor binding, at all sites of fibrosis; and (6) significant attenuation by lisinopril of collagen formation in the visceral pericardium of sham operated controls. CONCLUSIONS: In this model of tissue repair, increased AT1 receptor binding density is associated with ACE binding and fibrillar collagen formation that appears within sites of fibrous tissue formation, including myocardial infarction, endocardial fibrosis, foreign body (silk suture), and pericardiotomy. AT1 receptors may play a role in mediating the fibrogenic response to tissue injury in the rat heart. SN - 0008-6363 UR - https://www.unboundmedicine.com/medline/citation/7842454/Angiotensin_II_receptor_binding_following_myocardial_infarction_in_the_rat_ L2 - https://academic.oup.com/cardiovascres/article-lookup/doi/10.1093/cvr/28.11.1623 DB - PRIME DP - Unbound Medicine ER -