| First Author | Eichhorn B | Year | 2009 |
| Journal | Cardiovasc Res | Volume | 82 |
| Issue | 3 | Pages | 493-502 |
| PubMed ID | 19289377 | Mgi Jnum | J:162191 |
| Mgi Id | MGI:4818311 | Doi | 10.1093/cvr/cvp089 |
| Citation | Eichhorn B, et al. (2009) Impaired vascular function in small resistance arteries of LOX-1 overexpressing mice on high-fat diet. Cardiovasc Res 82(3):493-502 |
| abstractText | AIMS: LOX-1 is a major vascular receptor for oxidized low-density lipoprotein (oxLDL). In this study, we analysed the impact of LOX-1 overexpression and high dietary fat intake on vascular function in small resistance arteries. METHODS AND RESULTS: Relaxation of mesenteric arteries was measured using a wire myograph. Compared with the control group, mice overexpressing LOX-1 on a high-fat diet (FD) had preserved vascular smooth muscle relaxation, but impaired endothelium-dependent relaxation via NO. Vascular NO availability was decreased by exaggerated formation of reactive oxygen species and decreased endothelial NO synthase expression. Endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation via cytochrome P450 metabolites was increased in LOX-1 + FD animals, but did not completely compensate for the loss of NO. Currents of calcium-activated potassium channels with large conductance (BKCa channels) were measured by the voltage-clamp method. The BKCa current amplitudes were not altered in endothelial cells, but highly increased in vascular smooth muscle cells from resistance arteries of LOX-1-overexpressing mice on FD. BK(Ca) currents were activated by low-dose H2O2 and cytochrome P450 metabolites 11,12-EET and 14,15-EET as EDHF in control mice. CONCLUSION: LOX-1 overexpression and FD caused functional changes in endothelial and vascular smooth muscle cells of small resistance arteries. |
