PHARMACOGENETICS OF ACE INHIBITOR-ASSOCIATED ANGIOEDEMA

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目及 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 具体目标1。通过研究BK和P物质受体拮抗作用对ACE通路相关血管性水肿的持续时间和严重程度的影响，检验BK或P物质通过APP/DPPIV途径的异常降解导致人类ACE通路相关血管性水肿的假设。 具体目标2。根据BK和P物质降解表型，识别和表征血管紧张素转换酶抑制剂相关血管性水肿的激酶。

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.