The Endothelin-System and Hyperlipoproteinaemia are involved in the pathogenesis of arteriosclerosis. We investigated possible interactions between these systems. This work centres on the involvement of native and oxidatively modified Low-Density-Lipoprotein (nLDL, oxLDL) in the expression of genes of the Endothelin-System, the induction of apoptosis and the mediatory effects of Endothelin and Angiotensin on the uptake of oxLDL in HUVECs (Human Umbilical Vein Endothelial Cells). Endothelin-converting enzyme-1 (ECE-1) is induced by nLDL- and oxLDL (max. 100µg/ml). We investigated maximum effects in mRNA-expression after 1h, in protein-expression after 24h stimulation. ECE-1-induction was mediated via Angiotensin II - receptor 1 (AT1), Endothelin - receptor B (ETB), PKC, NOS and Ca2+-Ions. OxLDL and nLDL induced further the expression of ETB-mRNA in a time- and dose- dependent manner (max. 1 h, 100 µg/ml Lipoprotein). The induction of ETB - mRNA is dependent on PKC, Ca2+-Ions , Angiotensin II and the ETB-receptor itself. We were able to demonstrate an upregulation of ET1 - mRNA-expression and an induction of ET-1-peptide-production and -secretion by HUVEC after stimulation with nLDL and oxLDL. The induction of ppET-1-mRNA - expression is mediated by PKC, ETB- and AT1-receptor. Endothelin and Angiotensin II stimulate the uptake of oxLDL in HUVEC. We found no signs of apoptotic cell-death or enhanced DNA laddering even after maximal stimulation of HUVEC with nLDL or oxLDL (100 µg/ml, 24 h). Endothelin and Angiotensin induce the uptake of lipoproteins in HUVEC. They enable and potentiate interactions between Low-Density-Lipoproteins, Endothelin-1 and Angiotensin II within the scope of a circulus vitiosus of early arteriosclerosis.