on February 2, 2004
Published online before print February 2, 2004, doi: 10.1161/01.HYP.0000118017.02160.fa
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Submitted on October 17, 2003
From Department of Internal Medicine and Therapeutics (J.Y., K.Y., T.M., Y.S., N.N. M.N., T.O., M.H., T.Ma.), Osaka University Graduate School of Medicine, Suita, Japan, and Genome Information Research Center (J.Y., T.M., Y.S., N.N., T.Mi.), Osaka University, Suita, Japan. T.Ma. is currently at the Cardiovascular Division, Department of Internal Medicine, Hyogo College of Medicine. * To whom correspondence should be addressed. E-mail: kazuhiro{at}medone.med.osaka-u.ac.jp.
Abstract--Diastolic heart failure (DHF) has become a social burden; however, evidences leading to its therapeutic strategy are lacking. This study investigated effects of addition of angiotensin II type 1 receptor blocker (ARB) to angiotensin-converting enzyme inhibitor (ACEI) at advanced stage of DHF in hypertensive rats. Dahl salt-sensitive rats fed 8% NaCl diet from age 7 weeks served as DHF model, and those fed a normal chow served as control. The DHF model rats were arbitrarily assigned to 3 treatment regimens at age 17 weeks: ACEI (temocapril 0.4 mg/kg per day), combination of ACEI (temocapril 0.2 mg/kg per day) with ARB (olmesartan 0.3 mg/kg per day), or placebo. At age 17 weeks, this model represents progressive ventricular hypertrophy and fibrosis, relaxation abnormality, and myocardial stiffening. Data were collected at age 20 weeks. As compared with the monotherapy with ACEI, the addition of ARB induced more prominent suppression of ventricular hypertrophy and fibrosis, leading to suppression of myocardial stiffening, improvement of relaxation, and inhibition of hemodynamic deterioration. Such benefits were associated with greater decreases in reactive oxygen species (ROS) generation, macrophage infiltration, and gene expression of transforming growth factor (TGF)-
Revised on November 13, 2003
AT1 Receptor Blocker Added to ACE Inhibitor Provides Benefits at Advanced Stage of Hypertensive Diastolic Heart Failure
Junichi Yoshida;
1 and interleukin (IL)-1, but not with changes in gene expression of monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-
. Thus, ARB added to ACEI provides more benefits as compared with ACEI alone in DHF when initiated at an advanced stage. The additive effects are likely provided through more prominent suppression of ROS generation and inflammatory changes without effects on expression of MCP-1 and TNF-.
Key words: diastole • angiotensin II • angiotensin-converting enzyme • heart failure • oxidative stress
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