Key result
AT2 receptor-deficient mice treated with L-NAME showed worse left ventricular hypertrophy and more perivascular fibrosis than wild-type mice, indicating a protective effect of the AT2 receptor.
Why the study?
Does AT2 receptor deficiency worsen cardiac hypertrophy and fibrosis in L-NAME-induced chronic hypertension in mice?
Population
AT2 receptor-deficient (AT2 -/y) and wild-type (AT2 +/y) mice
Comparison
N-nitro-L-arginine methyl ester in drinking… vs Mice without L-NAME treatment
Design
Preclinical
Follow-up
4 weeks (3 weeks of L-NAME treatment)
Authors
Loading...
AT2 receptor protection in hypertensive remodeling is hypothesis-generating in mice; human relevance and therapeutic testing remain open.
Does AT2 receptor deficiency worsen cardiac hypertrophy and fibrosis in L-NAME-induced chronic hypertension in mice?
The AT2 receptor provides a protective effect against cardiac hypertrophy and fibrosis in a mouse model of L-NAME-induced chronic hypertension.
Groß et al. (2004) studied chronic hypertension. AT2 receptor deficiency (AT2 -/y) vs. Wild-type (AT2 +/y) was evaluated on left ventricular hypertrophy, perivascular fibrosis, and brain natriuretic peptide concentrations. AT2 receptor-deficient mice treated with L-NAME showed worse left ventricular hypertrophy and more perivascular fibrosis than wild-type mice, indicating a protective effect of the AT2 receptor.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: