title: Role of HDL in neutralizing the VLDL effect on endothelial dysfunction.
abstract: OBJECTIVE
  It has been reported that LDL inhibits endothelium-dependent relaxation (EDR) and that HDL can neutralize this effect. However, the atherogenic properties of VLDL have been so far difficult to demonstrate. Studies on VLDL are controversial, and nothing is known about the role of HDL on potential VLDL vascular actions. We examined the effect of human VLDLs on EDR, and the role of HDL in this system.
  
  
  METHODS
  VLDL (n=14) and LDL (n=6) were isolated from volunteer subjects. Normal HDL was obtained from one healthy donor. VLDL ability to inhibit ACh-induced vasorelaxation (10(-9)-10(-5)mM) on aortic rings previously precontracted by noradrenaline (10(-8)mM) was measured in the presence and absence of HDL.
  
  
  RESULTS
  ACh-induced maximal relaxation (R%) was mildly, but not significantly attenuated in the presence of VLDL (72±7%), while LDL caused a significant inhibition (60±10%, p<0.05) when compared to incubation in the absence of lipoproteins. VLDLs were subdivided into 2 groups depending on their cholesterol/triglyceride ratio: 0.18-0.22 (n=8) was considered typical and 0.10-0.15, rich in triglycerides (VLDLRT, n=6). Typical VLDL had no effect on EDR (p=0.38), however R% from VLDLRT was lower (54±7%, p<0.01) similar to the one obtained with LDL (p=0.32). HDL showed favorable effects on EDR inhibition induced by the presence of VLDLRT (p<0.05.).
  
  
  CONCLUSIONS
  Although typical VLDL did not cause endothelial dysfunction, triglyceride-enriched VLDL had inhibitory effect on EDR. It is proposed that alterations in VLDL composition would increase its atherogenic capacity. Moreover HDL appears to protect endothelium from VLDL action.
authors.affiliation: Laboratory of Lipids and Lipoproteins, Department of Clinical Biochemistry, Faculty of Pharmacy and Biochemistry, INFIBIOC, University of Buenos Aires, Buenos Aires C1113AAD, Argentina. vzago@ffyb.uba.ar
authors.forename: Valeria
authors.initials: V
authors.lastname: Zago
authors.forename: Susana
authors.initials: S
authors.lastname: Gorzalczany
authors.forename: Diego
authors.initials: D
authors.lastname: Lucero
authors.forename: Carlos
authors.initials: C
authors.lastname: Taira
authors.forename: Laura
authors.initials: L
authors.lastname: Schreier
mesh_terms: D000109:Acetylcholine / Q000737:chemistry; D000818:Animals; D001011:Aorta / Q000473:pathology; D050197:Atherosclerosis / Q000473:pathology; D008076:Cholesterol, HDL / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000473:pathology*; D006801:Humans; D066298:In Vitro Techniques; D008074:Lipoproteins / Q000737:chemistry; D008079:Lipoproteins, VLDL / Q000378:metabolism*; D008297:Male; D009638:Norepinephrine / Q000737:chemistry; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000378:metabolism*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D008076:Cholesterol, HDL; D008074:Lipoproteins; D008079:Lipoproteins, VLDL; D014280:Triglycerides; C030106:very low density lipoprotein triglyceride; D000109:Acetylcholine; D009638:Norepinephrine