Open AccessEffects of enalapril versus losartan on regression of volume overload-induced cardiac hypertrophy in rats.
Author(s) -
Marcel Ruzicka,
Baoxue Yuan,
F. H. H. Leenen
Publication year - 1994
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.90.1.484
Subject(s) - medicine , losartan , enalapril , cardiology , volume overload , afterload , preload , muscle hypertrophy , hemodynamics , pressure overload , angiotensin ii , heart failure , endocrinology , blood pressure , angiotensin converting enzyme , cardiac hypertrophy
The role of nonhemodynamic cardiac trophic mechanisms differs not only between different models of cardiac hypertrophy but also within the same model for development versus maintenance of cardiac hypertrophy. Our previous studies pointed to a major role for the renin-angiotensin system (RAS) as a cardiac trophic stimulus in the remodeling of the heart in response to volume overload by aortocaval shunt or minoxidil treatment.
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