Key result
Olmesartan treatment in spontaneously hypertensive rats increased ACE2 mRNA in the thoracic aorta fivefold compared with vehicle (P<0.05), whereas atenolol and hydralazine had no effect.
Why the study?
Does AT1 receptor blockade with olmesartan increase ACE2 and angiotensin-(1-7) expression and improve vascular remodeling in spontaneously hypertensive rats compared to other antihypertensives or vehicle?
Population
12-wk-old male spontaneously hypertensive rats (SHR), n=60
Comparison
Olmesartan 10 mg/kg/day for 2 weeks vs Atenolol 30 mg/kg/day, hydralazine 10 mg/kg/day…
Design
Preclinical
Follow-up
2 weeks
Authors
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Does not inform clinical ARB selection; leaves open whether ACE2 upregulation improves human vascular outcomes beyond BP control.
Does AT1 receptor blockade with olmesartan increase ACE2 and angiotensin-(1-7) expression and improve vascular remodeling in spontaneously hypertensive rats compared to other antihypertensives or vehicle?
Effect estimate: fivefold greater
p-value: p=<0.05
AT1 receptor blockade with olmesartan increases ACE2 and angiotensin-(1-7) expression and improves vascular remodeling in the thoracic aorta of spontaneously hypertensive rats, independent of blood pressure lowering.
Igase et al. (2005) studied Hypertension (n=60). Olmesartan vs. Atenolol, hydralazine, or vehicle was evaluated on ACE2 mRNA in the thoracic aorta (fivefold greater, p=<0.05). Olmesartan treatment in spontaneously hypertensive rats increased ACE2 mRNA in the thoracic aorta fivefold compared with vehicle (P<0.05), whereas atenolol and hydralazine had no effect.
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