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- W596192000 abstract "The aim of this study was to determine the chronic effects of Ang (1-7) on L-NAME-induced cardiac remodelling in both wildtype (WT), and AT2 knockout mice (AT2KO). Cardiac remodelling was induced by treatment with L-NAME (100mg/kg/day) for 4 weeks. Animals (n=10 in both WT and AT2KO, 16 wks old) were treated with L-NAME in combination with Ang (1-7) (24µg/kg/hr), the Mas receptor antagonist, A779 (48µg/kg/hr) and/or the COX inhibitor, indomethacin (2mg/kg/day). At the conclusion of treatment, hearts and aorta were removed to examine cardiovascular structure. Indices of cardiac (left ventricular to body weight ratio) hypertrophy were not influenced by any drug treatments. As expected, L-NAME significantly increased blood pressure (BP) and cardiac interstitial fibrosis in both WT and AT2KO mice. However, Ang (1-7) attenuated the increase in BP and interstitial fibrosis due to L-NAME by a similar magnitude in both WT and AT2KO. Indomethacin, but not A779 inhibited the ability of Ang (1-7) to prevent the L-NAME-induced hypertension implicating vasodilator prostaglandins in this effect. Thus, Ang (1-7) exhibits an anti-fibrotic effect that does not involve AT2R stimulation in this model. NHMRC (Australia)" @default.
- W596192000 created "2016-06-24" @default.
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- W596192000 date "2009-04-01" @default.
- W596192000 modified "2023-10-16" @default.
- W596192000 title "Cardiac anti‐fibrotic effect of Ang (1‐7) in L‐NAME‐treated mice does not involve AT2 receptor stimulation" @default.
- W596192000 doi "https://doi.org/10.1096/fasebj.23.1_supplement.935.3" @default.
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