Skip to main content
. Author manuscript; available in PMC: 2009 Apr 30.
Published in final edited form as: Exp Physiol. 2008 Mar 20;93(5):613–621. doi: 10.1113/expphysiol.2007.040246

Figure 4. The quantification of the Ang II metabolism (A) and Ang(1−7) formation (B) from the cardiac membranes of the wild-type, ACE−/− and ACE2−/− mice.

Figure 4

Angiotensin II metabolism was significantly enhanced in hearts of ACE−/− mice versus the wild-type (WT). The ACE2 inhibitor MLN4760 (A2I, 10 μm) reduced the metabolism of Ang II and the subsequent formation of Ang(1−7) in ACE−/− mice. Angiotensin II metabolism and Ang(1−7) generation were significantly reduced in the ACE2−/− mice. The ACE2 inhibitor (A2I) further attenuated the formation of Ang(1−7) in ACE2−/− mice. Data are the means ± s.e.m. *P < 0.05 versus control wild-type (CON); #P < 0.05 versus ACE−/− control; ϕP < 0.05 versus ACE2−/− control; n = 4.