title: Influence of sialic acid content of low-density lipoprotein particles on endothelium-dependent vasorelaxation in rabbit aorta.
abstract: 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 microg 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 microg 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 microg 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.
authors.affiliation: Department of Clinical Pharmacology, Centre for Cardiovascular Biology and Medicine, King's College, St. Thomas Hospital, Lambeth Palace Road, SE1 7EH, London, UK.
authors.forename: P D
authors.initials: PD
authors.lastname: Stratton
authors.forename: P J
authors.initials: PJ
authors.lastname: Lumb
authors.forename: G
authors.initials: G
authors.lastname: Paganga
authors.forename: M A
authors.initials: MA
authors.lastname: Crook
authors.forename: A
authors.initials: A
authors.lastname: Ferro
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology*; D001161:Arteriosclerosis / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood / Q000737:chemistry*; D008297:Male; D008875:Middle Aged; D019158:N-Acetylneuraminic Acid / Q000097:blood* / Q000494:pharmacology; D009439:Neuraminidase / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D011817:Rabbits; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D008077:Lipoproteins, LDL; D014665:Vasodilator Agents; D009599:Nitroprusside; D009439:Neuraminidase; D019158:N-Acetylneuraminic Acid; D000109:Acetylcholine