Inflammation causes dramatic changes in HDL composition and function. Therefore, we hypothesize that Endothelial Lipase (EL) induced alterations in the lipid and protein composition of HDL might yield HDL, with dramatically impaired endothelial function.In this thesis, HDL was modified by adenoviraly overexpressed EL in HepG2-cells. EL-HDL showed a markedly decreased total and relative phospholipid and triglyceride content when compared to control, lacZ-HDL. In addition, the relative protein and total cholesterol content were increased significantly in EL-HDL. The analysis of the HDL particle size by non-denaturing gradient gel electrophoresis (GGE) showed, that EL-HDL was smaller in size than lacZ-HDL.Western blotting revealed a relative change in paraoxonase1(PON1)-content in modified HDL. In some modifications, EL-HDL showed an increased PON1-content, whereas PON1 was decreased significantly in the majority of EL-HDL modifications. Regardless of the change in PON1-mass, the arylesterase activity assay, revealed a markedly reduced PON1 activity in all modifications. Further investigations showed no change in protein mass of apoM and apoA-I. However, sphingosine-1-phosphate (S1P) level was significantly decreased in EL-HDL.Wire myography measurements, using mouse aortic rings precontracted with norepinephrine (NE), revealed markedly diminished vasorelaxing capacity of EL- compared with lacZ-HDL. The measurement of nitrite concentrations in the supernatant of HAEC after incubation with modified HDL to determine the capacity of HDL to induce NO-release, showed a markedly decreased induction of NO-release by EL-HDL compared with lacZ-HDL. Based on these results we concluded, that EL-modification of human HDL markedly diminishes vasorelaxing capacity of HDL, most likely due to EL-mediated alterations in lipid and protein composition of HDL.