Peroxisome Proliferator-Activated Receptor-α and Receptor-γ Activators Prevent Cardiac Fibrosis in Mineralocorticoid-Dependent Hypertension
Why the study?
Do PPAR activators (rosiglitazone or fenofibrate) prevent cardiac remodeling in a DOCA-salt rat model of mineralocorticoid-dependent hypertension?
Population
Unilaterally nephrectomized 16-week-old Sprague-Dawley rats in a DOCA-salt model of…
Comparison
Rosiglitazone or fenofibrate for 3 weeks vs Control rats and untreated DOCA-salt rats
Design
Preclinical, randomly divided into 4 groups
Follow-up
3 weeks
Authors
Discussion
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Member takes
Implication
Should not change hypertension management; leaves open PPAR-mediated ET-1 effects on remodeling in mineralocorticoid models.
Structured PICO
Do PPAR activators (rosiglitazone or fenofibrate) prevent cardiac remodeling in a DOCA-salt rat model of mineralocorticoid-dependent hypertension?
P
Population
Unilaterally nephrectomized 16-week-old Sprague-Dawley rats (Uni-Nx) in a DOCA-salt model of mineralocorticoid-dependent hypertension overexpressing ET-1
I
Intervention
Rosiglitazone (PPAR-gamma activator, 5 mg/kg per day) or fenofibrate (PPAR-alpha activator, 100 mg/kg per day) for 3 weeks
C
Comparator
Control rats and untreated DOCA-salt rats
O
Outcome
Cardiac remodeling (including cardiac fibrosis, LV wall thickness, LV internal diameter, and prepro-ET-1 mRNA content)surrogate
PPAR-alpha and PPAR-gamma activators prevent cardiac fibrosis and concentric remodeling in a rat model of mineralocorticoid-induced hypertension, partly by decreasing ET-1 production.
Cite This Study
Iglarz et al. (2003) studied this question.