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Proposes a theoretical model of somatic ACE as a mechanosensor activated by shear stress, potentially explaining the clinical superiority of hydrophobic ACE inhibitors.
"Somatic" angiotensin I-converting enzyme (ACE) appears to be one of the evolutionary advances that made a closed circulation possible, and may have contributed to the Cambrian "explosion" of species approximately 540 million years ago. It also appears to be at the origin of a large number of common human diseases. A model is proposed in which the duplicated form of ACE ("somatic" ACE) functions as a mechanotransducer, defending downstream vessels and tissues from an increase in pressure. In the model, ACE senses shear stress (blood velocity) in regions of turbulent blood flow. An increase in shear stress strips an autoinhibitor tripeptide, FQP, from the N-terminal active site, thereby activating it. The C-terminal domain is constitutively activated by chloride. This model explains the clinical superiority of hydrophobic ACE inhibitors relative to hydrophilic ones.
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David W. Moskowitz (2002) studied this question.
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