Why the study?
Does bosentan reduce renin-angiotensin system activation (ACE, aldosterone) in monocrotaline-induced pulmonary hypertension rats?
Population
90 six-week-old male Sprague-Dawley rats weighing 200-250 g
Comparison
Bosentan 20 mg/kg/day administered by gavage… vs Monocrotaline 60 mg/kg subcutaneous injection…
Design
Preclinical
Follow-up
28 days
Key result
Bosentan treatment significantly decreased serum ACE concentrations (114.1 vs 190.7 U/L) and serum aldosterone levels on day 28 in rats with monocrotaline-induced pulmonary hypertension.
Authors
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Extends preclinical evidence on bosentan in experimental PH; leaves open translation to human disease.
Does bosentan reduce renin-angiotensin system activation (ACE, aldosterone) in monocrotaline-induced pulmonary hypertension rats?
Absolute Event Rate: 114.1% vs 190.7%
p-value: p=<0.05
Bosentan treatment attenuates the activation of the renin-angiotensin system, specifically reducing serum aldosterone and ACE levels, in a rat model of monocrotaline-induced pulmonary hypertension.
Kim et al. (2011) studied Monocrotaline-induced pulmonary hypertension (n=90). Bosentan vs. Monocrotaline alone (M group) and saline control (C group) was evaluated on Serum ACE concentration on day 28 (p=<0.05). Bosentan treatment significantly decreased serum ACE concentrations (114.1 vs 190.7 U/L) and serum aldosterone levels on day 28 in rats with monocrotaline-induced pulmonary hypertension.
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