Myocardiasl fibrosis

Role of angiotensin II and aldosterone

Karl Weber, C. G. Brilla, S. E. Campbell, E. Guarda, G. Zhou, K. Sriram

Research output: Contribution to journalArticle

108 Citations (Scopus)

Abstract

In this report we review the replacement (i.e., scarring) and reactive (i.e., perivascular and interstitial fibrosis) fibrous tissue responses found in the myocardium in response to effector hormones of the renin-angiotensin-aldosterone system. Experimental data are presented to indicate: a) endogenous or exogenous elevations in plasma angiotensin II are associated with acute cardiac myocyte necrosis and subsequent microscopic scarring; b) chronic elevations in plasma aldosterone (ALDO), relative to Na+ intake, are associated with a perivascular and interstitial fibrosis of the coronary and systemic circulations and are also seen in response to chronic administration of the mineralocorticoid hormone deoxycorticosterone (DOC); and c) chronic mineralocorticoid excess, due to ALDO or DOC, is associated with enhanced urinary K+ excretion, cardiac myocyte necrosis and scarring. Pharmacologic agents which interfere with these effector hormones (e.g., ACE inhibition and ALDO receptor antagonism) protect the myocardium against this pathologic structural remodeling created by the reactive and replacement (reparative) fibrosis. Evidence is also presented to indicate that chronic ACE inhibition is associated with a regression in reactive myocardial fibrosis. Based on these experimental findings we would suggest that clinical trials are indicated to address the prevention and regression of myocardial fibrosis - an important determinant of pathologic structural remodeling and abnormal myocardial stiffness.

Original languageEnglish (US)
Pages (from-to)107-124
Number of pages18
JournalBasic Research in Cardiology
Volume88
Issue numberSUPPL. 1
StatePublished - Jan 1 1993
Externally publishedYes

Fingerprint

Aldosterone
Angiotensin II
Fibrosis
Cicatrix
Desoxycorticosterone
Mineralocorticoids
Hormones
Cardiac Myocytes
Myocardium
Necrosis
Mineralocorticoid Receptors
Coronary Circulation
Renin-Angiotensin System
Clinical Trials

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Weber, K., Brilla, C. G., Campbell, S. E., Guarda, E., Zhou, G., & Sriram, K. (1993). Myocardiasl fibrosis: Role of angiotensin II and aldosterone. Basic Research in Cardiology, 88(SUPPL. 1), 107-124.

Myocardiasl fibrosis : Role of angiotensin II and aldosterone. / Weber, Karl; Brilla, C. G.; Campbell, S. E.; Guarda, E.; Zhou, G.; Sriram, K.

In: Basic Research in Cardiology, Vol. 88, No. SUPPL. 1, 01.01.1993, p. 107-124.

Research output: Contribution to journalArticle

Weber, K, Brilla, CG, Campbell, SE, Guarda, E, Zhou, G & Sriram, K 1993, 'Myocardiasl fibrosis: Role of angiotensin II and aldosterone', Basic Research in Cardiology, vol. 88, no. SUPPL. 1, pp. 107-124.
Weber K, Brilla CG, Campbell SE, Guarda E, Zhou G, Sriram K. Myocardiasl fibrosis: Role of angiotensin II and aldosterone. Basic Research in Cardiology. 1993 Jan 1;88(SUPPL. 1):107-124.
Weber, Karl ; Brilla, C. G. ; Campbell, S. E. ; Guarda, E. ; Zhou, G. ; Sriram, K. / Myocardiasl fibrosis : Role of angiotensin II and aldosterone. In: Basic Research in Cardiology. 1993 ; Vol. 88, No. SUPPL. 1. pp. 107-124.
@article{eb19817748c741e4be6aeace410f0a70,
title = "Myocardiasl fibrosis: Role of angiotensin II and aldosterone",
abstract = "In this report we review the replacement (i.e., scarring) and reactive (i.e., perivascular and interstitial fibrosis) fibrous tissue responses found in the myocardium in response to effector hormones of the renin-angiotensin-aldosterone system. Experimental data are presented to indicate: a) endogenous or exogenous elevations in plasma angiotensin II are associated with acute cardiac myocyte necrosis and subsequent microscopic scarring; b) chronic elevations in plasma aldosterone (ALDO), relative to Na+ intake, are associated with a perivascular and interstitial fibrosis of the coronary and systemic circulations and are also seen in response to chronic administration of the mineralocorticoid hormone deoxycorticosterone (DOC); and c) chronic mineralocorticoid excess, due to ALDO or DOC, is associated with enhanced urinary K+ excretion, cardiac myocyte necrosis and scarring. Pharmacologic agents which interfere with these effector hormones (e.g., ACE inhibition and ALDO receptor antagonism) protect the myocardium against this pathologic structural remodeling created by the reactive and replacement (reparative) fibrosis. Evidence is also presented to indicate that chronic ACE inhibition is associated with a regression in reactive myocardial fibrosis. Based on these experimental findings we would suggest that clinical trials are indicated to address the prevention and regression of myocardial fibrosis - an important determinant of pathologic structural remodeling and abnormal myocardial stiffness.",
author = "Karl Weber and Brilla, {C. G.} and Campbell, {S. E.} and E. Guarda and G. Zhou and K. Sriram",
year = "1993",
month = "1",
day = "1",
language = "English (US)",
volume = "88",
pages = "107--124",
journal = "Basic Research in Cardiology",
issn = "0300-8428",
publisher = "D. Steinkopff-Verlag",
number = "SUPPL. 1",

}

TY - JOUR

T1 - Myocardiasl fibrosis

T2 - Role of angiotensin II and aldosterone

AU - Weber, Karl

AU - Brilla, C. G.

AU - Campbell, S. E.

AU - Guarda, E.

AU - Zhou, G.

AU - Sriram, K.

PY - 1993/1/1

Y1 - 1993/1/1

N2 - In this report we review the replacement (i.e., scarring) and reactive (i.e., perivascular and interstitial fibrosis) fibrous tissue responses found in the myocardium in response to effector hormones of the renin-angiotensin-aldosterone system. Experimental data are presented to indicate: a) endogenous or exogenous elevations in plasma angiotensin II are associated with acute cardiac myocyte necrosis and subsequent microscopic scarring; b) chronic elevations in plasma aldosterone (ALDO), relative to Na+ intake, are associated with a perivascular and interstitial fibrosis of the coronary and systemic circulations and are also seen in response to chronic administration of the mineralocorticoid hormone deoxycorticosterone (DOC); and c) chronic mineralocorticoid excess, due to ALDO or DOC, is associated with enhanced urinary K+ excretion, cardiac myocyte necrosis and scarring. Pharmacologic agents which interfere with these effector hormones (e.g., ACE inhibition and ALDO receptor antagonism) protect the myocardium against this pathologic structural remodeling created by the reactive and replacement (reparative) fibrosis. Evidence is also presented to indicate that chronic ACE inhibition is associated with a regression in reactive myocardial fibrosis. Based on these experimental findings we would suggest that clinical trials are indicated to address the prevention and regression of myocardial fibrosis - an important determinant of pathologic structural remodeling and abnormal myocardial stiffness.

AB - In this report we review the replacement (i.e., scarring) and reactive (i.e., perivascular and interstitial fibrosis) fibrous tissue responses found in the myocardium in response to effector hormones of the renin-angiotensin-aldosterone system. Experimental data are presented to indicate: a) endogenous or exogenous elevations in plasma angiotensin II are associated with acute cardiac myocyte necrosis and subsequent microscopic scarring; b) chronic elevations in plasma aldosterone (ALDO), relative to Na+ intake, are associated with a perivascular and interstitial fibrosis of the coronary and systemic circulations and are also seen in response to chronic administration of the mineralocorticoid hormone deoxycorticosterone (DOC); and c) chronic mineralocorticoid excess, due to ALDO or DOC, is associated with enhanced urinary K+ excretion, cardiac myocyte necrosis and scarring. Pharmacologic agents which interfere with these effector hormones (e.g., ACE inhibition and ALDO receptor antagonism) protect the myocardium against this pathologic structural remodeling created by the reactive and replacement (reparative) fibrosis. Evidence is also presented to indicate that chronic ACE inhibition is associated with a regression in reactive myocardial fibrosis. Based on these experimental findings we would suggest that clinical trials are indicated to address the prevention and regression of myocardial fibrosis - an important determinant of pathologic structural remodeling and abnormal myocardial stiffness.

UR - http://www.scopus.com/inward/record.url?scp=0027323067&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027323067&partnerID=8YFLogxK

M3 - Article

VL - 88

SP - 107

EP - 124

JO - Basic Research in Cardiology

JF - Basic Research in Cardiology

SN - 0300-8428

IS - SUPPL. 1

ER -