PHARMACOGENETICS OF ACE INHIBITOR-ASSOCIATED ANGIOEDEMA

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Specific Aim 1. To test the hypothesis that aberrant degradation of either BK or substance P through the APP/DPPIV pathway contributes to ACE inhibitor-associated angioedema in humans, by investigating the effect of BK and substance P receptor antagonism on the duration and severity of ACE inhibitor-associated angioedema. Specific Aim 2. To identify and characterize kindreds with ACE inhibitor-associated angioedema according to BK and substance P degradation phenotype.