Lipids and endothelium‐dependent vasodilation—A review

Abstract

Studies using both in vitro and in vivo techniques have repeatedly shown that endothelium-dependent vasodilation (EDV) is impaired in different forms of experimental as well as human hypercholesterolemia. Clearly this impaired EDV can be reversed by lowering cholesterol levels by diet or medical therapy. Competitive blocking of L-arginine, changes in nitric oxide synthase activity, increased release of endothelin-1, and inactivation of nitric oxide due to superoxide ions all contribute to the impairment in EDV during dyslipidemia. The oxidation of low density lipoprotein, with its compound lysophosphatidylcholine, plays a critical role in these events. However, data on the role of triglycerides and fat-rich meals regarding EDV are not so consistent as data for cholesterol, although a view that the compositions of individual fatty acids and antioxidants are of major importance is emerging. Thus, this review shows that while impaired EDV is a general feature of hypercholesterolemia, the mechanisms involved and the therapeutic opportunities available still have to be investigated. Furthermore, discrepancies regarding the role of triglycerides and fat content in food may be explained by divergent effects of different fatty acids on the endothelium.

Endothelial dysfunction, inflammation, and insulin resistance: A focus on subjects at risk for type 2 diabetes

“…Each of these abnormalities are considered risk factors for type 2 diabetes and cardiovascular disease. Hypertriglyceridemia and low HDL cholesterol have been independently associated with endothelial dysfunction and inflammation [53].…”

The sterol response element binding protein regulates cyclooxygenase-2 gene expression in endothelial cells

“…Although cholesterol clearly impacts endothelial cell function (37,38), the direct effects of cholesterol on endothelial gene expression have not been investigated. We previously reported that cholesterol negatively regulates the expression of COX-2 in vascular endothelial cells (19).…”

Oxidized LDL and NO Synthesis as Biomarkers of Atherogenesis - Correlations with Metabolic Profile in Elderly

“…Ageing is characterized not only by a reduced arterial compliance and alteration of the contractile properties of the vascular wall, but also by endothelial dysfunction (Alvarez de Sotomayor, et al, 2005;Brandes et al, 2006). At present, there are several reasons to believe that in vivo NO synthesis from L-arginine could indeed be impaired in atherosclerosis, hypertension, dyslipidemia, diabetes, obesity, insulin resistance, metabolic syndrome, as well as in ageing (Lind, 2002;Laroia et al, 2003;Hsueh & Quinones, 2003;Holvoet et al, 2003Holvoet et al, , 2008aVickers et al, 2009;Park et al, 2009;Njajou et al, 2009;Huang, 2009;Park et al, 2011;Tabit et al, 2010). Recent studies support the fact that advancing age increases the LDL susceptibility to oxidation and decreases the nitric oxide availability and bioactivity .…”