Congenital immunity in patients with essential arterial hypertension and effectiveness of antihypertensive pharmacotherapy

The purpose of the study was to assess the parameters of innate immunity in patients with essential arterial hypertension and to establish a relationship with the effectiveness of antihypertensive pharmacotherapy.

Materials and methods. The study included 48 patients with essential arterial hypertension stage II, arterial hypertension 2 degree and hypertrophy of the left ventricular myocardium, which were divided into 2 groups: the first group (25 patients) - these are patients whose blood pressure reached the target values, and the second group (23 patients) are patients whose blood pressure did not reach the target values against the background of antihypertensive therapy (perindopril - 5 mg/day and amlodipine - 5 mg/day) (group 2). Indicators of 18 healthy donors were used as a comparison group (control group).

Results. In patients with essential arterial hypertension of group 1, compared with the control group, the concentration of IL-1α, IL-6, IL-8, IL-10, IL-1 receptor antagonist, IL-2, C₄- and C_5a-components of the complement system and factor H is significantly higher and the level of C₃ is lower-component of the complement system. In patients with essential arterial hypertension of group 2, more pronounced changes in the cytokine link of the immunity and the complement system were established before the start of antihypertensive therapy. After the antihypertensive therapy in patients with essential arterial hypertension of the 1^st group in the blood plasma, the concentration of TNF, IL-1α, IL-8, IL-10, IL-1 receptor antagonist significantly decreased, but not to the values of the control group, and in patients of the 2^nd group, the effectiveness of antihypertensive therapy in correcting parameters innate immunity was found to be less effective.

Conclusion. Revealing the participation of innate immunity indicators in the formation of arterial hypertension opens up new possibilities for the pathogenetic therapy of this disease and developing measures to prevent or level the damage to target organs.

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