Expression of LOX-1 in spontaneously hypertensive rat carotid atherosclerotic lesions

Oxidized low-density lipoprotein (Ox-LDL) has been implicated in the pathogenesis of atherosclerosis (Proc. Natl. Acad. Sci. U. S. A. 84 (1987) 5928, N. Engl. J. Med. 320 (1989) 915, J. Clin. Invest. 88 (1991) 1785). It is hypothesized that Ox-LDL is trapped by a scavenger receptor on the surface of macrophages, resulting in the formation of foam cells and subsequent atherosclerotic lesion (Nature (Lond.) 343 (1990) 531). Ox-LDL is also reported to be internalized and degraded in the endothelium, attenuates the endothelium-dependent vasodilatory response through reduced production of nitric oxide (NO), and induces endothelial expression of leucocyte adhesion molecules (J. Clin. Invest. 90 (1992) 1138) and smooth-muscle growth factors (Nature 362 (1993) 801). In this study, we examined the vascular expression of lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) in hypercholesterolaemic SHR-SP/Izm rats by immunohistochemistry. Hypercholesterolaemic SHR-SP/Izm rats were produced by feeding SHR-SP/Izm a high fat and high cholesterol diet (H.F.C.) containing 0.023% N^G-nitro-L-arginine (L-NNA) and 1% NaCl in their drinking water (Clin. Exp. Pharmacol. Physiol. 24 (1997) 344). We found that LOX-1 expression was low in the common carotid artery of WKY/Izm, whereas it was markedly up-regulated in those of SHR-SP/Izm rats and hypercholesterolaemic SHR-SP/Izm rats. These results indicated that LOX-1 expression in the carotid artery were up-regulated not only in hypertensive rats but in hypercholesterolaemic rats, which may be involved in the impaired endothelium-dependent vasodilatation in these rats.