Relation of C-Reactive Protein to Oxidative Stress and to Endothelial Activation in Essential Hypertension

Background C-reactive protein (CRP) predicts cardiovascular outcome. Oxidative stress is considered to be involved in endothelial alteration. We hypothesized that in essential hypertension (EH), oxidative stress, as measured by 8-iso-prostaglandin-F2α (8-iso-PGF2α), should be associated with increased CRP and endothelial activation, as evaluated by soluble intercellular adhesion molecule–1 (ICAM-1) and vascular adhesion molecule–1 (VCAM-1) plasma levels. Methods In 83 subjects with mild EH and in 50 healthy control subjects we measured, in basal conditions, plasma levels of hs-CRP, 8-iso-PGF2α, ICAM-1 and VCAM-1, and tumor necrosis factor–α (TNF-α). Results Subjects with EH had higher levels of 8-iso-PGF2α (P< .0001), CRP (P< .001), ICAM-1 and VCAM-1 (P< .001), and TNF-α (P< .001) than did control subjects. We divided successively EH according to CRP values (<1, 1–3, >3 mg/L), and we observed increasing and significantly different levels of the endothelial parameters and of TNF-α along with increasing CRP. Linear analysis of correlation pointed out significant correlation of CRP with 8-iso-PGF2α (r = 0.730, P< .001), ICAM-1 and VCAM-1 (r = 0.642 and 0.468, P< .001 respectively), and TNF-α (r = 0.609, P< .001). Multiple regression analysis using CRP as a dependent variable confirmed the relationship of CRP with systolic blood pressure (β 0.216, P = 0.039) and with 8-iso-PGF2α (β 0.602, P = .0001). Conclusions Our data demonstrate that in EH, inflammatory molecules such as CRP and TNF-α are increased and related to both oxidative stress and endothelial activation.