Key result
Bosentan treatment decreased serum ACE concentrations and serum aldosterone levels on day 28 in rats with monocrotaline-induced pulmonary hypertension.
Why the study?
Does bosentan reduce renin-angiotensin system activation (ACE, aldosterone) in monocrotaline-induced pulmonary hypertension rats?
Does bosentan reduce renin-angiotensin system activation (ACE, aldosterone) in monocrotaline-induced pulmonary hypertension rats?
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.
Answers are grounded in this paper and cite their sources.
Extends preclinical evidence on bosentan in experimental PH; leaves open translation to human disease.
Background: Pulmonary artery hypertension is characterized by persistent increase of vascular resistance, and is associated with right ventricle failure. We investigated changes of plasma renin, serum aldosterone, angiotensin converting enzyme (ACE) concentrations, ACE gene expressions and protein contents after bosentan treatment. Methods: Six-week-old male Sprague-Dawley rats were divided into three groups: control (C) group, monocrotaline (M) group, and bosentan (B) group.
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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 decreased serum ACE concentrations and serum aldosterone levels on day 28 in rats with monocrotaline-induced pulmonary hypertension.
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