Abstract
Hypertension in its origin is a heterogeneous and multisystemic disease. Evaluation of oxidative stress activity based on the level of 8-iso-PgF2α, proinflammatory activity based on tumour necrosis factor-α, its type I soluble receptor, and C-reactive protein levels is relevant for further understanding of pathogenesis of hypertension and improvement of the early diagnostics of heart failure. 186 hypertensive patients were observed during a 2-months course of treatment, aged 30 to 65 years. Serum levels of 8-iso-PgF2α (n = 34), tumour 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 clinically healthy individuals, aged 27 to 55 years. Hypertensive patients enrolled into the study were randomized into three groups that received different protocols of combined anti-hypertensive therapy: I clinical group – а combination of bisoprolol and indapamid, II – а combination of lacidipine and candesartan, III – а combination of fosinopril sodium and hydrochlorothiazide. On the background of combined antihypertensive therapy, we observed favourable dynamics of 8-iso-PgF2α, tumour necrosis factor-α and its type I soluble receptor, and C-reactive protein levels. Taking into account the insignificance of the correlations revealed, a one-factor dispersion analysis was applied which allowed us to determine the influence of the grade and duration of hypertension on the dynamics of the studied parameters. It has been found that the grade of hypertension is related to an increase in TNF-α and 8-iso-PgF2α serum levels, but not in TNF-α type I soluble receptor, and the duration of hypertension is related to an increase in C-reactive protein, TNF-α and its type I soluble receptor levels, with no relation to the level of 8-iso-PgF2α. Thus, oxidative stress possibly promotes the activation of potentially damaging immune mechanisms mediated by proinflammatory cytokines, nonspecific inflammation and drives the further progression of lesions in the target organs.
Highlights
Hypertension occupies one of the leading places in the structure of cardiac pathology and presents a complex medical and social problem considering its high prevalence and the early development of complications
Tumour necrosis factor-α (TNF-α) deserves special attention in the context of hypertension. This is due to the fact that, as shown by experiments and an insignificant number of clinical studies, hemodynamic stress caused by increased blood pressure (BP) is one of the stimuli to increase production and release of pro-inflammatory cytokines, including tumour necrosis factor-α (TNF-α), into the bloodstream (Goldhaber et al, 1996; Grainger, 2007)
Analysis of the activity of proinflammatory cytokines showed a significant increase in the levels of TNF-α in patients with hypertension compared to control: 187 ± 18.1 vs 13.2 ± 3.4 pg/mL, respectively (P < 0.001)
Summary
Hypertension occupies one of the leading places in the structure of cardiac pathology and presents a complex medical and social problem considering its high prevalence and the early development of complications. The role of immune inflammatory activation mediated by proinflammatory cytokines, systemic inflammation and oxidative stress (OS) in the pathogenesis of cardiovascular diseases, including hypertension, has been actively studied (Bautista et al, 2005; Mahmud & Feel, 2005). Tumour necrosis factor-α (TNF-α) deserves special attention in the context of hypertension This is due to the fact that, as shown by experiments and an insignificant number of clinical studies, hemodynamic stress caused by increased blood pressure (BP) is one of the stimuli to increase production and release of pro-inflammatory cytokines, including TNF-α, into the bloodstream (Goldhaber et al, 1996; Grainger, 2007). TNF-α promotes apoptosis of cardiomyocytes, and activates metalloproteinases and depresses the expression of their inhibitors, promoting cardiac remodeling (Li et al, 2000; Haider et al, 2002) and eventually leading to cardiac dysfunction
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