RAAS AND FIBRINOLYSIS: ACEI AND PE5I

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 为了验证这样一种假设，即通过给予NO供体增加cGMP的形成或通过给予磷酸二酯酶抑制剂防止cGMP的降解，将在不减少t-PA释放的情况下，增强ACE抑制对炎性细胞因子、纤溶标志物和胰岛素敏感性的有利作用。测试通过给予磷酸二酯酶抑制剂他达拉非增加cGMP将增强ACE抑制对代谢综合征患者活性PAI-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.