Key result
Treatment with a specific angiotensin II type 1 receptor antagonist completely prevented L-NAME-induced increases in TGF-beta1 and extracellular matrix protein gene expression and cardiac fibrosis.
Why the study?
Does angiotensin II type 1 receptor blockade or TGF-beta neutralization prevent cardiac fibrosis in rats with chronic NO synthesis inhibition?
Population
Normal rats administered oral N(omega)-nitro-L-arginine methyl ester (L-NAME) to induce cardiac fibrosis
Comparison
Specific angiotensin II type 1 receptor… vs Hydralazine
Design
Preclinical
Authors
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AT1 blockade may attenuate fibrosis in NO-deficient rat models; leaves open clinical translation to human hypertension or HF.
Does angiotensin II type 1 receptor blockade or TGF-beta neutralization prevent cardiac fibrosis in rats with chronic NO synthesis inhibition?
Early induction of TGF-beta1 via the angiotensin II type 1 receptor plays a major role in the development of cardiac fibrosis induced by chronic NO synthesis inhibition in rats.
Tomita et al. (1998) studied Cardiac fibrosis. Angiotensin II type 1 receptor antagonist and neutralizing antibody against TGF-beta vs. Hydralazine was evaluated on Cardiac fibrosis and mRNA levels of TGF-beta1 and extracellular matrix proteins. Treatment with a specific angiotensin II type 1 receptor antagonist completely prevented L-NAME-induced increases in TGF-beta1 and extracellular matrix protein gene expression and cardiac fibrosis.
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