Signals for the remodeling of the cardiac interstitium in systemic hypertension

Karl Weber, C. G. Brilla, J. S. Janicki

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Cardiac myocyte growth is the common denominator in myocardial hypertrophy irrespective of the hypertrophic stimulus. The hypertrophic remodeling of the myocardium may or may not also include the growth of nonmyocyte cells, thereby creating the potential for heterogeneity in tissue growth. Hypertrophy, therefore, need not be a uniform process, especially if trophic factors responsible for myocyte and nonmyocyte growth are independent of one another. To examine this hypothesis further, we determined the relative importance of hemodynamic and hormonal factors in augmenting ventricular mass and cardiac fibroblast-induced collagen accumulation in several rat (Sprague-Dawley) models of arterial hypertension: renovascular hypertension (RHT), infrarenal aorta banding (IRB), and chronic aldosterone (ALDO) administration. Elevations in arterial pressure were comparable in each, whereas circulating angiotensin II (Ang II) and ALDO were dissimilar: in RHT, each was increased; with IRB they were normal; and with chronic ALDO, Ang II was suppressed whereas ALDO was increased. We reasoned that because of the in-series arrangement of the ventricles, where only the left ventricle (LV) experienced an elevation in systolic pressure, the right ventricle (RV) served as a negative control regarding hemodynamic factors. Relative to the in-parallel arrangement of the ventricles, provided by the coronary circulation, the RV served as a positive control for circulating hormones. In comparison to their age- and sex-matched controls, quantitative morphometry indicated that (a) comparable left ventricular hypertrophy in each model; (b) right ventricular hypertrophy was not present in any model; (c) a reactive interstitial fibrosis and perivascular fibrosis of intramyocardial coronary arteries were present in RHT and ALDO, but not in IRB; and (d) this fibrous tissue response was present in both the normotensive RV and the hypertensive LV. Thus, ventricular systolic pressure, not circulating hormones, determines myocyte growth and ventricular mass whereas elevations in coronary perfusion pressure, together with elevations in circulating Ang II and/or ALDO, determine the involvement of cardiac fibroblasts and collagen accumulation. We therefore conclude that trophic factors regulating myocyte and nonmyocyte growth are indeed independent of one another and can account for tissue heterogeneity in the structural remodeling of the myocardium in various form of hypertension.

Original languageEnglish (US)
JournalJournal of Cardiovascular Pharmacology
Volume17
Issue numberSUPPL. 2
StatePublished - 1991
Externally publishedYes

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Aldosterone
Heart Ventricles
Hypertension
Renovascular Hypertension
Growth
Angiotensin II
Muscle Cells
Aorta
Hypertrophy
Myocardium
Fibrosis
Collagen
Fibroblasts
Hemodynamics
Hormones
Blood Pressure
Right Ventricular Hypertrophy
Coronary Circulation
Left Ventricular Hypertrophy
Ventricular Pressure

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

Signals for the remodeling of the cardiac interstitium in systemic hypertension. / Weber, Karl; Brilla, C. G.; Janicki, J. S.

In: Journal of Cardiovascular Pharmacology, Vol. 17, No. SUPPL. 2, 1991.

Research output: Contribution to journalArticle

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