Myocardial fibrosis and pathologic hypertrophy in the rat with renovascular hypertension

Karl Weber, Joseph S. Janicki, Ruth Pick, Joseph Capasso, Piero Anversa

Research output: Contribution to journalArticle

110 Citations (Scopus)

Abstract

An abnormal elevation in collagen concentration or myocardial fibrosis occurs in the hypertrophied left ventricle of the rat with renovascular hypertension (RHT). The structural nature and functional consequences of this fibrosis and the mechanisms involved in its appearance were reviewed for various phases of hypertrophy. Within days after the onset of renal ischemia, type I collagen messenger ribonucleic acid is expressed. An interstitial fibrosis follows, characterized by an increased dimension of existing perimysial fibers and the appearance of fibrillar collagen in spaces previously devoid of collagen, together with a perivascular fibrosis of intramyocardial coronary arteries. These expressions of myocardial fibrosis are associated with an increase in diastolic and systolic myocardial stiffness. Endomyocardial fibrosis serves to further increase diastolic stiffness while myocytes encircled by fibrillar collagen become atrophic. Each of these consequences of myocardial fibrosis reduce myocyte length-dependent force generation. At 32 weeks of RHT there is an obvious diastolic and systolic dysfunction of the ventricle together with heart failure that includes ventricular dilatation, wall thinning and reduced ejection fraction. The mechanisms involved in mediating fibrosis in RHT appear to be multiple. Myocyte necrosis and fibroblast proliferation have been associated with elevated circulating angiotensin II. Necrosis in RHT was not seen with captopril pretreatment or in the hypertension and hypertrophy that accompanied infrarenal aorta banding. An alteration in coronary artery permeability may be responsible for the perivascular fibrosis that is not seen with captopril pretreatment. Thus in RHT, the hemodynamic status of the ventricle determines myocyte hypertrophy while the elevation in circulating angiotensin II is responsible for the remodeling of nonmyocyte compartments, including the appearance of myocardial fibrosis. Pathologic hypertrophy and heart failure in RHT are therefore the result of primary events that occur within the interstitial and vascular compartments of the myocardium.

Original languageEnglish (US)
Pages (from-to)1-7
Number of pages7
JournalThe American Journal of Cardiology
Volume65
Issue number14
DOIs
StatePublished - Apr 3 1990

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Renovascular Hypertension
Hypertrophy
Fibrosis
Muscle Cells
Fibrillar Collagens
Captopril
Angiotensin II
Coronary Vessels
Necrosis
Collagen
Heart Failure
Endomyocardial Fibrosis
Collagen Type I
Heart Ventricles
Blood Vessels
Aorta
Dilatation
Permeability
Myocardium
Ischemia

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Myocardial fibrosis and pathologic hypertrophy in the rat with renovascular hypertension. / Weber, Karl; Janicki, Joseph S.; Pick, Ruth; Capasso, Joseph; Anversa, Piero.

In: The American Journal of Cardiology, Vol. 65, No. 14, 03.04.1990, p. 1-7.

Research output: Contribution to journalArticle

Weber, Karl ; Janicki, Joseph S. ; Pick, Ruth ; Capasso, Joseph ; Anversa, Piero. / Myocardial fibrosis and pathologic hypertrophy in the rat with renovascular hypertension. In: The American Journal of Cardiology. 1990 ; Vol. 65, No. 14. pp. 1-7.
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