Infusion of Ang(1-7) and A-779 (400 ng/kg/min, s.c.) alone or combined for 6 weeks does not prevent uterus atrophy or inhibit the body weight gain of OVX rats. A-779 markedly elevates serum bone specific alkaline phosphatase (BALP), telopeptides of collagen type I (CTX), tartarate resistant acid phosphatase (TRAcP 5b), osteocalcin (OC) and urinary deoxypyridinoline (DPD). Infusion of Ang(1-7) and/or A-779 does not significantly change serum minerals concentrations in sham or OVX groups. A-779 in the OVX animals does not change AngII, Ang(1-7), AT1R, AT2R, ACE, ACE-2, Mas receptor, RANKL and OPG proteins expressions in relation to OVX group, while AngII (P < 0.05), AT1R (P < 0.05), ACE (P < 0.01) and RANKL (P < 0.01) expressions are significantly higher and Ang(1-7), AT2R, ACE-2, MasR and OPG are significantly (P < 0.01) lower than sham group. Blocking of the G-protein coupled receptor (Mas) by A-779 markedly abolishes Ang(1-7) favorable effects on bone health suggesting the vital role of Mas receptor in mediating Ang(1-7) osteo-protective effects[1]. Inhibition of Ang1-7 cascade by A-779 (400 ng/kg/min) significantly eradicates captopril protective effects on bone metabolism, mineralization and micro-structure. A-779 also restores OVX effects on RANKL expression and ACE-1/AngII/AT1R cascade and down-regulates OPG expression and ACE-2/Ang1-7/Mas pathway[2].
