Key result
In dogs with pacing-induced CHF, ET(A) receptor antagonism lowered systemic and pulmonary vascular resistance, attenuated ANP elevation, and improved sodium excretion compared to untreated controls.
Why the study?
Does chronic selective oral ET(A) receptor antagonism improve cardiorenal and endocrine responses in a canine model of pacing-induced congestive heart failure?
Population
12 conscious dogs undergoing 21 days of pacing-induced congestive heart failure (CHF)
Comparison
A-127722 (ET receptor antagonist) 5 mg/kg oral… vs Untreated control group
Design
Preclinical
Follow-up
21 days
Authors
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ET(A) antagonism may improve hemodynamics and natriuresis in canine CHF; hypothesis-generating and leaves open human translation.
Does chronic selective oral ET(A) receptor antagonism improve cardiorenal and endocrine responses in a canine model of pacing-induced congestive heart failure?
In a canine model of pacing-induced heart failure, chronic oral ET(A) receptor antagonism improved systemic and pulmonary hemodynamics and attenuated sodium retention, suggesting a potential therapeutic role in heart failure.
Borgeson et al. (1998) studied congestive heart failure (n=12). ET(A) receptor antagonist (A-127722) vs. untreated control was evaluated on cardiorenal and endocrine responses. In dogs with pacing-induced CHF, ET(A) receptor antagonism lowered systemic and pulmonary vascular resistance, attenuated ANP elevation, and improved sodium excretion compared to untreated controls.
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