Key result
Angiotensin-(1-7) prevented ANG II-mediated phosphorylation of ERK1/2 and Rho kinase in a dose-dependent manner via Mas receptors, while stimulating STAT3 and 5a/b phosphorylation via AT1 receptors.
Population
Anaesthetized male Sprague-Dawley rats
Comparison
Angiotensin- in increasing doses (0.08 to 800… vs Angiotensin II alone, basal values, or with…
Design
Preclinical
Follow-up
5 min
Authors
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May inform cardiac remodeling mechanisms; animal data leave open human translation and therapeutic relevance.
Angiotensin-(1-7) exerts a dual role in the heart by stimulating STAT phosphorylation via AT1 receptors and inhibiting ANG II-induced ERK1/2 and Rho kinase activation via Mas receptors, suggesting a protective mechanism against cardiac remodeling.
Giani et al. (2008) studied this question. Angiotensin-(1-7) vs. Angiotensin II alone was evaluated on ERK1/2, Rho kinase, STAT3 and STAT5a/b phosphorylation. Angiotensin-(1-7) prevented ANG II-mediated phosphorylation of ERK1/2 and Rho kinase in a dose-dependent manner via Mas receptors, while stimulating STAT3 and 5a/b phosphorylation via AT1 receptors.
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