Remodeling of the rat right and left ventricles in experimental hypertension.
- 1 December 1990
- journal article
- research article
- Published by Ovid Technologies (Wolters Kluwer Health) in Circulation Research
- Vol. 67 (6), 1355-1364
- https://doi.org/10.1161/01.res.67.6.1355
Abstract
Pathological left ventricular hypertrophy in renovascular hypertension is associated with the accumulation of fibrillar collagen within the extracellular space and around intramyocardial coronary arteries. Even though the angiotensin converting enzyme inhibitor captopril was previously found to attenuate this interstitial and perivascular fibrosis, the relative importance of arterial and ventricular systolic pressures versus circulating angiotensin II (AII) and aldosterone (AL) in promoting hypertrophy and collagen accumulation in renovascular hypertension is uncertain. By drawing on the in-parallel arrangement of the right and left ventricles, with respect to their coronary circulation, and the in-series mechanical alignment of the ventricles, with a pressure-overloaded left and a normotensive right ventricle, this study sought to address this uncertainty. Three models of experimental hypertension, each having a different circulating AII and AL profile, were examined and compared with their controls: renovascular hypertension, where both AII and AL are increased; infrarenal aorta banding, where AII and AL are normal; and a chronic infusion of AL, where AII is suppressed or normal and AL is increased. In renovascular hypertension, as well as with AL, we found a significant rise in the interstitial collagen volume fraction and perivascular collagen area of the pressure-overloaded, hypertrophied left ventricle as well as the normotensive, nonhypertrophied right ventricle. This remodeling was not seen in either ventricle with infrarenal aorta banding despite comparable systemic hypertension and left ventricular hypertrophy. Thus, in experimental arterial hypertension in the rat, myocyte and nonmyocyte compartments of the myocardium are under separate controls: myocyte hypertrophy is most closely related to ventricular loading while circulating AII and AL, acting alone or in concert with other humoral factors, regulate the accumulation of collagen within the right and left ventricles.This publication has 28 references indexed in Scilit:
- Changes in Nonmyocyte Tissue Composition Associated with Pressure Overload of Hypertrophic Human HeartsPathology - Research and Practice, 1989
- Physiologic Versus Pathologic Hypertrophy and the Pressure-Overloaded MyocardiumJournal of Cardiovascular Pharmacology, 1987
- Morphometric analysis of collagen network and plasma perfused capillary bed in the myocardium of rats during evolution of cardiac hypertrophyBasic Research in Cardiology, 1986
- True versus immunoreactive angiotensin II in human plasma.Hypertension, 1985
- Hemodynamic versus adrenergic control of cat right ventricular hypertrophy.JCI Insight, 1985
- Connective tissue content and myocardial stiffness in pressure overload hypertrophy A combined study of morphologic, morphometric, biochemical, and mechanical parametersBasic Research in Cardiology, 1983
- Aldosterone infusion into the rat and dose-dependent changes in blood pressure and arterial ionic transport.Hypertension, 1982
- Mineralocorticoid binding in cultured smooth muscle cells and fibroblasts from rat aortaJournal of Steroid Biochemistry, 1981
- Collagen synthesis in development and reversal of cardiac hypertrophy in spontaneously hypertensive ratsThe American Journal of Cardiology, 1979
- Cell proliferation during cardiac growthThe American Journal of Cardiology, 1973