RAAS AND FIBRINOLYSIS: ACEI AND PE5I

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 中心，不一定是研究者的机构。 为了验证这一假设，即增加cGMP，无论是通过给予NO供体增加其形成或通过给予磷酸二酯酶抑制剂防止其降解，将增强ACE抑制剂对代谢综合征活动性个体的炎性细胞因子、纤溶标志物和胰岛素敏感性的有利作用，而不减少t-PA释放。在代谢综合征患者中，检验通过给予磷酸二酯酶抑制剂他达拉非增加cGMP将增强ACE抑制对活性派-1抗原和胰岛素敏感性以及t-PA活性的有利作用的假设。

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. To test the hypothesis that increasing the cGMP, either by increasing its formation by administering an NO donor or by preventing its degradation by administering a phosphodiesterase inhibitor, will enhance the favorable effects of ACE inhibition on inflammatory cytokines, markers of fibrinolysis and insulin sensitivity in individuals with the metabolic syndromeactivity without decreasing t-PA release. Test the hypothesis that increasing cGMP through administration of the phosphodiesterase inhibitor tadalafil will enhance the favorable effects of ACE inhibition on active PAI-1 antigen and insulin sensitivity, as well as on t-PA activity, in individuals with the metobolic syndrome.