Key result
Olmesartan treatment inhibited cardiac hypertrophy independently of blood pressure reduction in renin-overexpressing mice, whereas hydralazine did not.
Why the study?
Does olmesartan inhibit cardiac hypertrophy independently of blood pressure reduction in mice overexpressing renin?
Does olmesartan inhibit cardiac hypertrophy independently of blood pressure reduction in mice overexpressing renin?
Olmesartan inhibits cardiac hypertrophy independently of its blood pressure-lowering effects in a renin-overexpressing mouse model, potentially through enhancement of the ACE2/Ang(1-7)/Mas axis.
Does not alter clinical practice; extends evidence of BP-independent ARB effects to renin-overexpressing mice.
Enhanced renin-angiotensin activity causes hypertension and cardiac hypertrophy. The angiotensin (Ang)-converting enzyme (ACE)2/Ang(1-7)/Mas axis pathway functions against Ang II type 1 receptor (AT1R) signaling. We investigated whether olmesartan (Olm), an AT1R blocker, inhibits cardiac hypertrophy independently of blood pressure, and evaluated the potential mechanisms. The 3- to 4-month-old male mice overexpressing renin in the liver (Ren-Tg) were given Olm (5 mg/kg/d) and hydralazine (Hyd) (3.5 mg/kg/d) orally for 2 months. Systolic blood pressure was higher in the Ren-Tg mice than in wild-type littermates. Olm and Hyd treatments lowered systolic blood pressure to the same degree. However, cardiac hypertrophy, evaluated by echocardiography, heart weight, cross-sectional area of cardiomyocytes, and gene expression, was inhibited by only Olm treatment, but not by Hyd. Olm treatment reversed decreased gene expressions of ACE2 and Mas receptor of Ren-Tg mice and inhibited enhanced NADPH oxidase (Nox)4 expression and reactive oxygen species, whereas Hyd treatment had no influence on them. These findings indicate that Olm treatment inhibits cardiac hypertrophy independently of blood pressure, not only through its original AT1R blockade but partly through enhancement of ACE2/Ang(1-7)/Mas axis and suppression of Nox4 expression.
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Tanno et al. (2016) studied Hypertension and cardiac hypertrophy. Olmesartan vs. Hydralazine (3.5 mg/kg/d) was evaluated on Cardiac hypertrophy (evaluated by echocardiography, heart weight, cross-sectional area of cardiomyocytes, and gene expression). Olmesartan treatment inhibited cardiac hypertrophy independently of blood pressure reduction in renin-overexpressing mice, whereas hydralazine did not.
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