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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 1. Metabolism of Ang I by cardiac membranes.

Figure 1

Angiotensin I was incubated with cardiac membranes (50 μg) for 120 min at 37°C and the metabolites separated by HPLC. A, Ang I was hydrolysed primarily to Ang(1−9) in the heart membranes from wild-type mice. B, increased metabolism of Ang I results in a peak of Ang(1−4) in the heart membranes of ACE−/− mice. C, addition of the chymase inhibitor chymostatin (10 μm) reduced the peak of Ang(1−4) and increased the peak of Ang(1−9) in ACE−/− mice. D, addition of the ACE2 inhibitor MLN4760 (10 μm) did not attenuate the formation of Ang(1−9). E, the carboxypeptidase A inhibitor benzylsuccinate reduced the peak of Ang(1−9) and increased the level of Ang I. F, Ang I was hydrolysed primarily to Ang(1−9) in the heart membranes from ACE2−/− mice. The HPLC metabolism results are representative of four separate experiments.