Abstract

Background. Cardiovascular diseases remain the leading cause of mortality in patients with metabolic syndrome, while arterial hypertension is one of the key factors of cardiovascular risk. Recent studies indicate an important role of immune mechanisms, particularly pro-inflammatory reactions and alterations in the humoral immune response, in the development of vascular dysfunction. However, the specific features of immune disturbances in comorbid pathology remain insufficiently understood, which determines the relevance of this study.
Aim: to investigate humoral immune mechanisms and evaluate their involvement in the pathogenesis of arterial hypertension associated with metabolic syndrome.
Materials and Methods. The study was performed on 48 non-linear Wistar rats and 108 spontaneously hypertensive rats (SHR) of both sexes. Metabolic syndrome was induced by long-term administration of a fructose-enriched diet. Observations were conducted at weeks 7–8 and 16–17 of the experiment. Serum levels of circulating immune complexes as well as concentrations of immunoglobulins IgA, IgG, and IgM were determined.
Results. In SHR rats, a significant increase in circulating immune complexes and a decrease in immunoglobulin concentrations were detected already at the early stages of the experiment compared with Wistar rats. During the experiment, further accumulation of circulating immune complexes was observed along with a persistent decrease in IgA and IgG levels, whereas IgM levels remained relatively stable. Induced metabolic syndrome intensified these changes: animals with comorbid pathology demonstrated a more pronounced increase in circulating immune complexes and a decrease in all major immunoglobulin classes.
Conclusion. Arterial hypertension, especially when combined with metabolic syndrome, is accompanied by significant disturbances of the humoral immune response manifested by increased formation of circulating immune complexes and decreased immunoglobulin levels