Tags

Type your tag names separated by a space and hit enter

Regional changes in angiotensin II receptor density after experimental myocardial infarction.
J Mol Cell Cardiol. 1996 Feb; 28(2):429-40.JM

Abstract

The plasma and cardiac renin-angiotensin systems may be activated after myocardial infarction. The myocardium may therefore be exposed to increased concentrations of angiotension II, which may contribute to myocardial injury. The purpose of this study was to identify the potential sites of action of angiotensin II in the infarcted heart. Myocardial infarction was induced in rats by left coronary artery ligation, and the hearts were removed for study after 18 h, 7 days, or 8 months. The regional ventricular angiotensin II receptor density was assessed by [125I](Sar1,Ile8)angiotensin II binding and quantitative autoradiography. The [125I](Sar1,Ile8)angiotensin II binding was unchanged at 18 h, but was increased at 7 days in the infarcted region of the left ventricle (73.2 +/- 3.2 amol/mm2, mean +/- S.E.M.) compared with the non-infarcted region (1.6 +/- 0.2 amol/mm2, P < 0.0001) and with the left ventricular myocardium of sham-operated control animals (1.3 +/- 0.1 amol/mm2, P < 0.0001). The increased [125I](Sar1,Ile8)angiotensin II binding density was still present, but diminished, at 8 months after coronary ligation (49.0 +/- 5.7 amol/mm2, P < 0.0001 v control, P = 0.0058 v 7-day infarcts). The increased binding of [125I](Sar1,Ile8)angiotensin II was antagonised by losartan, an AT1 receptor antagonist, but not by an AT2 receptor antagonist. Microautoradiography of [125I](Sar1,Ile8) angiotensin II, and assessment of collagen deposition using picrosirius staining and immunostaining demonstrated that the regional increase in AT1 receptor density in the infarcted region of myocardium was associated with fibroblast infiltration and collagen deposition. The infarct scar and the cardiac fibroblasts within it express high levels of angiotension II receptors and therefore represent potential targets for the actions of angiotensin II after myocardial infarction.

Authors+Show Affiliations

Department of Histochemistry, Royal Postgraduate Medical School, London, UK.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8729073

Citation

Lefroy, D C., et al. "Regional Changes in Angiotensin II Receptor Density After Experimental Myocardial Infarction." Journal of Molecular and Cellular Cardiology, vol. 28, no. 2, 1996, pp. 429-40.
Lefroy DC, Wharton J, Crake T, et al. Regional changes in angiotensin II receptor density after experimental myocardial infarction. J Mol Cell Cardiol. 1996;28(2):429-40.
Lefroy, D. C., Wharton, J., Crake, T., Knock, G. A., Rutherford, R. A., Suzuki, T., Morgan, K., Polak, J. M., & Poole-Wilson, P. A. (1996). Regional changes in angiotensin II receptor density after experimental myocardial infarction. Journal of Molecular and Cellular Cardiology, 28(2), 429-40.
Lefroy DC, et al. Regional Changes in Angiotensin II Receptor Density After Experimental Myocardial Infarction. J Mol Cell Cardiol. 1996;28(2):429-40. PubMed PMID: 8729073.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regional changes in angiotensin II receptor density after experimental myocardial infarction. AU - Lefroy,D C, AU - Wharton,J, AU - Crake,T, AU - Knock,G A, AU - Rutherford,R A, AU - Suzuki,T, AU - Morgan,K, AU - Polak,J M, AU - Poole-Wilson,P A, PY - 1996/2/1/pubmed PY - 1996/2/1/medline PY - 1996/2/1/entrez SP - 429 EP - 40 JF - Journal of molecular and cellular cardiology JO - J Mol Cell Cardiol VL - 28 IS - 2 N2 - The plasma and cardiac renin-angiotensin systems may be activated after myocardial infarction. The myocardium may therefore be exposed to increased concentrations of angiotension II, which may contribute to myocardial injury. The purpose of this study was to identify the potential sites of action of angiotensin II in the infarcted heart. Myocardial infarction was induced in rats by left coronary artery ligation, and the hearts were removed for study after 18 h, 7 days, or 8 months. The regional ventricular angiotensin II receptor density was assessed by [125I](Sar1,Ile8)angiotensin II binding and quantitative autoradiography. The [125I](Sar1,Ile8)angiotensin II binding was unchanged at 18 h, but was increased at 7 days in the infarcted region of the left ventricle (73.2 +/- 3.2 amol/mm2, mean +/- S.E.M.) compared with the non-infarcted region (1.6 +/- 0.2 amol/mm2, P < 0.0001) and with the left ventricular myocardium of sham-operated control animals (1.3 +/- 0.1 amol/mm2, P < 0.0001). The increased [125I](Sar1,Ile8)angiotensin II binding density was still present, but diminished, at 8 months after coronary ligation (49.0 +/- 5.7 amol/mm2, P < 0.0001 v control, P = 0.0058 v 7-day infarcts). The increased binding of [125I](Sar1,Ile8)angiotensin II was antagonised by losartan, an AT1 receptor antagonist, but not by an AT2 receptor antagonist. Microautoradiography of [125I](Sar1,Ile8) angiotensin II, and assessment of collagen deposition using picrosirius staining and immunostaining demonstrated that the regional increase in AT1 receptor density in the infarcted region of myocardium was associated with fibroblast infiltration and collagen deposition. The infarct scar and the cardiac fibroblasts within it express high levels of angiotension II receptors and therefore represent potential targets for the actions of angiotensin II after myocardial infarction. SN - 0022-2828 UR - https://www.unboundmedicine.com/medline/citation/8729073/Regional_changes_in_angiotensin_II_receptor_density_after_experimental_myocardial_infarction_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2828(96)90039-5 DB - PRIME DP - Unbound Medicine ER -