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. 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 2. The quantification of the Ang I metabolism (A) and Ang(1−9) formation (B) from cardiac membranes of wild-type, ACE−/− and ACE2−/− mice.

Figure 2

Angiotensin I metabolism was significantly enhanced in hearts of ACE−/− mice versus the wild-type (WT). Addition of the chymase inhibitor chymostatin (CHM, 10 μm) did not alter Ang I metabolism (A), but increased Ang(1−9) (B) in ACE−/− mice. The ACE2 inhibitor MLN4760 in the presence of chymostatin (CHM-A2I, 10 μm) did not alter Ang I or Ang(1−9) metabolism compared with CHM alone. Addition of the carboxypeptidase A benzylsuccinate (BSC, 10 μm) significantly reduced the metabolism of Ang I and subsequent formation of Ang(1−9). Data are means + s.e.m. *P < 0.05 versus control (CON); #P < 0.05 versus chymostatin (CHM); n = 4.