Influence of sialic acid content of low-density lipoprotein particles on endothelium-dependent vasorelaxation in rabbit aorta

• Published in: Atherosclerosis Vol. 154; no. 2; pp. 285 - 290
• Main Authors: Stratton, Paula D, Lumb, Peter J, Paganga, George, Crook, Martin A, Ferro, Albert
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Ireland Ltd 01.02.2001; Elsevier
• Subjects: Acetylcholine - pharmacology; Adult; Animals; Aorta, Thoracic - drug effects; Aorta, Thoracic - physiology; Arteriosclerosis - blood; Arteriosclerosis - etiology; Arteriosclerosis - physiopathology; Atherosclerosis (general aspects, experimental research); Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiology; Humans; Lipoproteins, LDL - blood; Lipoproteins, LDL - chemistry; Low-density lipoprotein; Male; Medical sciences; Middle Aged; N-Acetylneuraminic Acid - blood; N-Acetylneuraminic Acid - pharmacology; Neuraminidase - pharmacology; Nitroprusside - pharmacology; Rabbits; Sialic acid; Vascular endothelium; Vasodilation - drug effects; Vasodilation - physiology; Vasodilator Agents - pharmacology; Vasorelaxation; Low-density lipoprotein; Vascular endothelium; Sialic acid; Vasorelaxation; Pathogenesis; Rabbit; Cardiovascular disease; Lagomorpha; Endothelium; Vascular disease; Lipoprotein LDL; Vertebrata; Vasomotricity; Mammalia; Animal; Atherosclerosis
• ISSN: 0021-9150; 1879-1484
• DOI: 10.1016/S0021-9150(00)00479-2

Low-density lipoprotein (LDL) concentration in plasma is an important predictor for atherosclerosis, and desialylated LDL has been proposed to be particularly atherogenic. Atherosclerosis is also associated with vascular endothelial dysfunction. We therefore wished to test the hypothesis that removal of sialic acid residues from LDL increases its ability to inhibit endothelium-dependent vasorelaxation. We studied vasorelaxant responses to acetylcholine (ACh) in isolated rabbit aortic rings as a model of endothelium-dependent relaxation, in the presence or absence of LDL treated either with saline or with neuraminidase, to cleave sialic acid residues. Vasorelaxant responses to ACh were inhibited by 300 μg protein per ml saline-treated LDL ( E max 77.5±4.5 vs. 89.7±2.2% in the absence of LDL, P<0.05). This inhibitory effect was not altered by neuraminidase treatment of LDL. In contrast, 300 μg protein per ml LDL, either saline- or neuraminidase-treated, did not affect vasorelaxant responses to the endothelium-independent dilator sodium nitroprusside. We found no correlation between sialic acid content of saline-treated LDL and its ability to inhibit endothelium-dependent vasorelaxation, in rabbit aortic rings, at a concentration of 300 μg protein per ml. Our results therefore suggest that sialic acid content is not an important determinant of the effect of LDL on vascular endothelium-dependent relaxation.