Angiotensin 1-7 (Ang-(1-7)) acetate, an endogenous heptapeptide from the renin-angiotensin system (RAS), exhibits cardioprotective effects through anti-inflammatory and anti-fibrotic activities in cardiac cells. It inhibits purified canine ACE activity (IC50 = 0.65 μM) and modulates kinin-induced vasodilation by hindering ACE and facilitating nitric oxide release. This compound also prevents Ang II-induced proliferation and hypertrophy in smooth muscle cells and demonstrates antiangiogenic and growth-inhibitory effects on the endothelium [1] [2] [3].

Angiotensin 1-7 (Ang-(1-7)) opposes angiotensin II by inhibiting growth in cultured vascular smooth muscle cells, in contrast to angiotensin II's growth-stimulating effect at equal molar concentrations[2], counteracts the myofibroblast phenotype induced by methylglyoxal-modified albumin (MGA) in NRK-52E cells by mitigating prolonged TGF-β-ERK pathway activation[4], and operates through the Mas receptor (MasR), diverging from the angiotensin II/angiotensin II type 1 receptor (AT1R) pathway, facilitating anti-inflammatory, vasodilatory, and neuroprotective actions[5].

Daily administration of Angiotensin 1-7 (Ang-(1-7)) at doses ranging from 0.01 to 0.06 mg/kg significantly alleviates Di-nitrochlorobenzene (DSS)-induced colitis. This treatment notably decreases the colitis-associated phosphorylation of p38, ERK1/2, and Akt[3].