Review article
Fibrosis in hypertensive heart disease: role of the renin-angiotensin-aldosterone system

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Clinical evidence

The essential criterion in defining hypertensive heart disease (HHD) is a greater than normal heart mass in the absence of a cause other than arterial hypertension. It is now accepted, however, that besides left ventricular hypertrophy (LVH), alterations in myocardial structure as listed below account for loss of tissue homogeneity and pathologic remodeling that appears in HHD:

  • Cellular alterations

  • Cardiomyocytes

  •  Hypertrophy, atrophy, apoptosis, necrosis

  • Noncardiomyocytes

  •  Hyperplasia and apoptosis

Role of angiotensin II in myocardial fibrosis

Various lines of evidence support a role for ANGII as a critical candidate factor to induce myocardial fibrosis in HHD.

Summary

Structural homogeneity of cardiac tissue is governed by mechanical and humoral factors that regulate cell growth, apoptosis, phenotype, and extracellular matrix turnover. ANGII has endocrine, autocrine, and paracrine properties that influence the behavior of cardiac cells and matrix by AT1 receptor binding. Various paradigms have been suggested, including ANGII-mediated up-regulation of collagen types I and III formation and deposition in cardiac conditions, such as HHD. A growing body of

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