Angiotensina-(1-9) disminuye el remodelamiento cardiovascular hipertensivo independiente de los niveles de ECA y de angiotensina II

background: the angiotensin i converting enzyme 2 (ace2) counteracts the deleterious effects of ace and ang ii through angiotensin (ang) -(1-9) rather than ang-(1-7). in addition, it is not clear whether ang-(1-9) is effective in the reversal of hypertensive cardiovascular remodeling (cvrm) in rats with ace gene polymorphism. objective: to determine the effect of ang-(1-9) in the prevention of hypertensive cvrm in rats with genetically determined levels of ace and ang ii. methods: in normotensive homozygous lewis (ll) and brown norway (bn) rats hypertension was induced by the goldblatt 2 kidney-1 pinch model. after 4 weeks, rats were randomized to receive ang- (1-9) (602 ng / kg min) or the co administration of ang- (19) + a779 (100 ng / kg min, a mas receptor antagonist of ang- (1-7)) for 14 days. sham operated rats were used as controls. we determined body mass (bm), systolic blood pressure (sbp), ventricular mass (vm), cardiomyocyte area (ca), area and thickness of the aortic media (atm, ttm), lv total collagen volume fraction (fvct), type i collagen protein levels (col i) in the aorta (ao) and macrophage infiltration in lv and ao, through its specific molecule ed1 (ed1-ao, ed1-vi). results: continuous administration of ang- (1-9) significantly decreased sbp, vm, ca, tcvf, col i, ttm, and ed1 in the aorta and left ventricle of hypertensive rats. this effect was not inhibited by the antagonist a779. ace polymorphism did not modify the response to treatment. conclusion: ang- (1-9) effectively reduced hypertension induced cvrm independent of ace gene polymorphism. this effect was not mediated by ang- (1-7).