Increased levels of low-density lipoproteins are well-established risk factors of endothelial dysfunction and the metabolic syndrome. In this study, we evaluated the effect of native low- density lipoprotein (nLDL) and oxidized LDL (oxLDL) on the expression of genes of the renin-angiotensin system (angiotensin- converting enzyme, ACE; angiotensin II type 1 receptor, AT1) and their receptors (low-density lipoprotein receptor, LDLR; lectin-like oxLDL receptor LOX-1; toll-like receptor 4, TLR4) in primary cultures of human umbilical vein endothelial cells. ACE and AT1 expression was significantly increased after stimulation with nLDL and oxLDL. LDL receptor was induced in response to nLDL and oxLDL after 1 h. OxLDL receptor LOX-1 showed a maximum induction after 7 h. Increased LOX-1 protein expression in response to oxLDL could be blocked by a LOX-1- specific antibody. TLR4 expression was increased by nLDL and oxLDL as well. We conclude that LDL and oxLDL can activate the renin-angiotensin system and their receptors LDLR, LOX-1 and TLR4 in human endothelial cells. These data suggest a novel link between hypercholesterolemia and hypertension in patients with the metabolic syndrome.