title: Effects of chronic arterial hypertension on constitutive and induced intercellular adhesion molecule-1 expression in vivo.
abstract: Recent reports indicate that bacterial endotoxin (lipopolysaccharide) and cytokines elicit a more profound increase in the surface expression of intercellular adhesion molecule-1 (ICAM-1) in cultured endothelial cells derived from spontaneously hypertensive (SHR) versus normotensive Wistar-Kyoto rats (WKY). Our objective in this study was to characterize and compare in vivo ICAM-1 expression in SHR and WKY under basal conditions and after 5 hours of endothelial cell activation with either lipopolysaccharide (5 mg/kg i.p.) or tumor necrosis factor-alpha (TNF-alpha; 1, 5, and 10 micrograms/kg i.p.). ICAM-1 expression was quantified in different tissues by the double-radiolabeled monoclonal antibody technique. When constitutive (baseline) ICAM-1 expression was corrected for endothelial cell surface area, significantly higher values were noted in SHR than WKY but only in splanchnic organs. Lipopolysaccharide and TNF-alpha elicited significant increases in ICAM-1 expression in all tissues of both WKY and SHR. However, the magnitude of the lipopolysaccharide-induced ICAM-1 upregulation in heart, stomach, skeletal muscle, and brain was significantly lower in SHR than WKY. A similar blunted ICAM-1 upregulation was noted in the stomach of SHR after administration of 5 micrograms/kg TNF-alpha. The differences in induced ICAM-1 expression between SHR and WKY do not appear to be due to differences in endothelial cell surface area or plasma glucocorticoid levels. These results suggest that chronic arterial hypertension results in altered ICAM-1 expression on the endothelium, which may contribute to the abnormal inflammatory responses associated with this disease.
authors.affiliation: Department of Physiology, LSU Medical Center, Shreveport 71130-3932, USA.
authors.forename: S
authors.initials: S
authors.lastname: Komatsu
authors.forename: J
authors.initials: J
authors.lastname: Panés
authors.forename: J M
authors.initials: JM
authors.lastname: Russell
authors.forename: D C
authors.initials: DC
authors.lastname: Anderson
authors.forename: V R
authors.initials: VR
authors.lastname: Muzykantov
authors.forename: M
authors.initials: M
authors.lastname: Miyasaka
authors.forename: D N
authors.initials: DN
authors.lastname: Granger
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D001921:Brain / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D002908:Chronic Disease; D004727:Endothelium / Q000187:drug effects / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism; D006727:Hormone Antagonists / Q000494:pharmacology; D006973:Hypertension / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology; D015735:Mifepristone / Q000494:pharmacology; D018482:Muscle, Skeletal / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000276:immunology / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D015815:Cell Adhesion Molecules; D006727:Hormone Antagonists; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D015735:Mifepristone; D007703:Peptidyl-Dipeptidase A