Open AccessComparative Effects of Losartan, Captopril, and Enalapril on Murine Acute Myocarditis Due to Encephalomyocarditis Virus
Author(s) -
M Araki,
Tsugiyasu Kanda,
Shoichi Imai,
Tadashi Suzuki,
Katsuyuki Murata,
Isao Kobayashi
Publication year - 1995
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-199507000-00010
Subject(s) - enalapril , losartan , captopril , medicine , myocarditis , viral myocarditis , heart failure , angiotensin converting enzyme , inflammation , pharmacology , angiotensin ii , endocrinology , receptor , blood pressure
Losartan, a recently developed nonpeptide angiotensin II (AII) receptor antagonist, was orally administered for 14 days to mice with viral myocarditis, beginning 7 days after encephalomyocarditis virus inoculation. The angiotensin-converting enzyme inhibitors (ACEI) captopril and enalapril were also administered in the same manner to compare the therapeutic effects of these three drugs on the degree of myocarditis, acute heart failure, and left ventricular (LV) hypertrophy. Heart weight and the heart weight/body weight ratio were reduced by losartan (60 mg/kg/day) and captopril (7.5 mg/kg/day), but not by enalapril (1 mg/kg/day). LV wall thickness and cavity dimension were decreased in the losartan and captopril groups. Captopril reduced both myocardial necrosis and inflammation, whereas enalapril reduced myocardial necrosis but not inflammation. However, none of the studied losartan doses (1.2, 12, 60 mg/kg/day) influenced myocardial necrosis and inflammation resulting from viral infection. Thus, specific blockade of AII is beneficial in congestive heart failure (CHF) and LV hypertrophy but is not effective in viral-evoked inflammation and injury.