October 1, 2001Journal of Hypertension
Ventricular production of natriuretic peptides and ventricular structural remodeling in hypertensive heart failure
Why the study?
Does AT1R or alpha1-receptor blockade prevent LV fibrosis and normalize BNP gene expression in a rat model of hypertensive heart failure?
Population
Dahl salt-sensitive rats, n=34
Comparison
Doxazosin or candesartan cilexetil vs Untreated hypertensive heart failure model
Design
Preclinical
Authors
Discussion
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Implication
AT1R blockade may attenuate fibrosis-linked BNP expression in hypertensive HF models; leaves open clinical translation pending human trials.
Structured PICO
Does AT1R or alpha1-receptor blockade prevent LV fibrosis and normalize BNP gene expression in a rat model of hypertensive heart failure?
P
Population
Dahl salt-sensitive rats (hypertensive heart failure model), n=34 (24 for serial changes, 5 for doxazosin, 5 for candesartan cilexetil)
I
Intervention
Doxazosin (1 mg/kg per day) or candesartan cilexetil (1 mg/kg per day)
C
Comparator
Untreated hypertensive heart failure model (implied)
O
Outcome
Serial changes in LV geometry, histology, and ANP and BNP mRNA levelssurrogate
In a hypertensive heart failure rat model, BNP gene expression is enhanced by LV fibrosis and late-stage hypertrophy dependent on AT1R-mediated signaling, rather than initial compensatory hypertrophy.
Cite This Study
Sakata et al. (2001) studied this question.