Effect of valsartan and fosinopril on catecholamine-induced cardiac hypertrophy
Abstract
"AIM:
To study the influence of angiotensin (Ang) II receptor antagonist (AT1) valsartan and angiotensin-converting enzyme (ACE) inhibitor fosinopril on the cardiac hypertrophy induced by catecholamine.
METHODS:
A cardiac hypertrophy model was produced by i.p. norepinephrine (NE) 1.5 mg.kg-1.d-1 x 15 d. The animals were divided into four groups: 1) control (sodium chloride), 2) NE, 3) NE + fosinopril, 4) NE + valsartan. Fosinopril ig 15 mg.kg-1.d-1 x 15 d, valsartan ig 30 mg.kg-1.d-1 x 15 d.
RESULTS:
Valsartan ig 30 mg.kg-1.d-1 x 15 d and fosinopril ig 15 mg.kg-1.d-1 x 15 d prevented left ventricular hypertrophy induced by NE and decreased the content of collagen in myocardium; valsartan and fosinopril both elevated the myosin ATPase activity, Na+, K(+)-ATPase activity in membrane, and Ca(2+)-ATPase activity in mitochondrias. Apoptosis was induced in cardiomyocytes by catecholamine. Valsartan and fosinopril both inhibited apoptosis, and no significant differences were found in the apoptotic index between the two treatment groups.
CONCLUSION:
Valsartan and fosinopril prevent the remodeling of cardiac hypertrophy induced by norepinephrine. Cardiac myocyte apoptosis may play a key role in the heart remodeling."
Keywords:
To study the influence of angiotensin (Ang) II receptor antagonist (AT1) valsartan and angiotensin-converting enzyme (ACE) inhibitor fosinopril on the cardiac hypertrophy induced by catecholamine.
METHODS:
A cardiac hypertrophy model was produced by i.p. norepinephrine (NE) 1.5 mg.kg-1.d-1 x 15 d. The animals were divided into four groups: 1) control (sodium chloride), 2) NE, 3) NE + fosinopril, 4) NE + valsartan. Fosinopril ig 15 mg.kg-1.d-1 x 15 d, valsartan ig 30 mg.kg-1.d-1 x 15 d.
RESULTS:
Valsartan ig 30 mg.kg-1.d-1 x 15 d and fosinopril ig 15 mg.kg-1.d-1 x 15 d prevented left ventricular hypertrophy induced by NE and decreased the content of collagen in myocardium; valsartan and fosinopril both elevated the myosin ATPase activity, Na+, K(+)-ATPase activity in membrane, and Ca(2+)-ATPase activity in mitochondrias. Apoptosis was induced in cardiomyocytes by catecholamine. Valsartan and fosinopril both inhibited apoptosis, and no significant differences were found in the apoptotic index between the two treatment groups.
CONCLUSION:
Valsartan and fosinopril prevent the remodeling of cardiac hypertrophy induced by norepinephrine. Cardiac myocyte apoptosis may play a key role in the heart remodeling."