RAAS AND FIBRINOLYSIS: ACEI AND PE5I

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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. 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.