Key result
In a rat model of high-output heart failure, acute inhibition of the angiotensin converting enzyme or angiotensin II type 1 receptors restored ANP release in response to volume expansion (p<0.01).
Why the study?
Does acute inhibition of the renin-angiotensin system restore ANP release and diuretic response to volume expansion in a rat model of high-output heart failure?
Population
Rat model of shunt-induced high-output heart failure
Comparison
Acute inhibition of angiotensin converting… vs Rats with aortocaval shunt without angiotensin…
Design
Preclinical
Follow-up
acute
Authors
Loading...
Angiotensin inhibition may blunt ANP release to volume load in experimental HF; leaves open clinical relevance in patients.
Does acute inhibition of the renin-angiotensin system restore ANP release and diuretic response to volume expansion in a rat model of high-output heart failure?
p-value: p=<0.01
In a rat model of high-output heart failure, acute inhibition of the renin-angiotensin system restores the impaired ANP release and diuretic response to volume expansion, suggesting an additional mechanism for the benefits of these drugs in heart failure.
Roland Willenbrock (1999) studied Shunt-induced high-output heart failure. Acute inhibition of the angiotensin converting enzyme or angiotensin II type 1 receptors vs. Controls (rats without shunt or without inhibition) was evaluated on ANP release and renal excretory function in response to volume expansion (p=<0.01). In a rat model of high-output heart failure, acute inhibition of the angiotensin converting enzyme or angiotensin II type 1 receptors restored ANP release in response to volume expansion (p<0.01).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: