Antihypertensive treatment effects on systemic inflammation, oxidative stress and proinflammatory cytokines

Abstract

Hypertension in its origin is a heterogeneous and multisystemic disease. Evaluatation of the oxidative stress activity based on the level of 8-iso-PgF2α, of proinflammatory cytokines based on tumor necrosis factor-α and its type I soluble receptor and C-reactive protein is relevant for further understanding of pathogenesis of hypertension and improvement of the early diagnostics of heart failure.186 hypertensive patients have been observed during the 2-months course of treatment, aged 30 to 65 years. The serum levels of 8-iso-PgF2α (n = 34), tumor necrosis factor-α and its type I soluble receptor were determined by ELISA before and after course of treatment. C-reactive protein level was determined by biochemical method. The control group included 16 practically healthy individuals, aged 27 to 55 years. Hypertensive patients enrolled into study had been randomized into 3 arms that received different protocols of combined anti-hypertensive therapy. I clinical group – а combination of a bisoprolol and indapamid, II – а combination of a lacidipine and candesartan, III – а combination of а fosinopril sodium and hydrochlorothiazide. On the background of combined antihypertensive therapy, we observed favorable dynamics of 8-iso-PgF2α, tumor necrosis factor-α and its type I soluble receptor and C-reactive protein. Taking into account the insignificance of the correlations revealed, a one-factor dispersion analysis was applied which allows to determine with certainty the influence of the grade and duration of hypertension on the dynamics of the studied indices levels. It has been found that the grade of hypertension is related to the increase in TNF-α and 8-iso-PgF2α serum levels, but not on to TNF-α type I soluble receptor, and the duration of hypertension is related to the increase in activity of the C-reactive protein, TNF-α and its type I soluble receptor, with no relation to the level of 8-iso-PgF2α. Thus, oxidative stress possibly promotes the activation of potentially damaging immune mechanisms mediated by pro-inflammatory cytokines, nonspecific inflammation and drives the further progression of the target organs lesions.