Population
Male Wistar rats
Comparison
N-nitro-l-arginine methyl ester alone or l-NAME… vs Control group
Design
Preclinical, divided randomly
Follow-up
4 weeks
Authors
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Supports distinct mitochondrial versus fibrotic remodeling mechanisms in NO-deficient hypertension; hypothesis-generating for BP-independent antifibrotic strategies.
In a rat model, chronic NO synthase inhibition induces hypertension and mitochondrial remodeling that is reversible with captopril, while interstitial fibrosis appears directly related to NO insufficiency rather than elevated blood pressure.
Rossi et al. (2003) studied this question.
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