Alamandine is generated by catalysis of Ang A via ACE2 or directly from Angiotensin 1-7 (Ang-(1-7)). Derived from angiotensin II (Ang II) by Ang II-converting enzyme 2 (ACE2), it shows vasodilating (thus protective) properties. Ang (1-7) can be decarboxylated to a peptide called Alamandine. Alamandine is also an endogenous peptide identified in human blood.
Alamandine elevates cAMP concentration in primary endothelial and mesangial cells, also suggesting Gs coupling.
Alamandine decreases secretion, expression, and blood levels of leptin. Alamandine induced expression of iNOS and plasminogen activator inhibitor-1 (PAI-1) in adipose tissue and isolated adipocytes.

Alamandine (0.15 ?μL/h; administered by mini-osmotic pumps; for 6 weeks) treatment ameliorates hypertension and impaires left ventricle (LV) function in SHRs. Also decreases the mass gains of heart and lung in SHRs, suppresses cardiomyocyte cross-sectional area expansion, and inhibits the mRNA levels of atrial natriuretic peptide and brain natriuretic peptide.