Renin-angiotensin system mediated mechanisms: cardioreparation and cardioprotection
Open Access
- 1 September 2000
- Vol. 84 (90001), 18i-19
- https://doi.org/10.1136/heart.84.suppl_1.i18
Abstract
A number of changes occur within the myocardial structure during the development of LVH. There is a tremendous increase in myocyte size in patients with dilated cardiomyopathy, hypertensive heart disease, coronary artery disease or post-myocardial infarction. The major physiological stimulus for myocytes to undergo hypertrophy is mechanical stress, or stretch, either provided by increased preload, or increased afterload, or a combined increase in both.Keywords
This publication has 5 references indexed in Scilit:
- Advanced Hypertensive Heart Disease in Spontaneously Hypertensive RatsHypertension, 1996
- Collagen Metabolism in Cultured Adult Rat Cardiac Fibroblasts: Response to Angiotensin II and AldosteroneJournal of Molecular and Cellular Cardiology, 1994
- Impaired diastolic function and coronary reserve in genetic hypertension. Role of interstitial fibrosis and medial thickening of intramyocardial coronary arteries.Circulation Research, 1991
- Stretching cardiac myocytes stimulates protooncogene expression.Journal of Biological Chemistry, 1990
- Collagen network remodelling and diastolic stiffness of the rat left ventricle with pressure overload hypertrophyCardiovascular Research, 1988