IMMUNOLOGICAL ASPECTS OF VASCULAR DYSFUNCTION AND REMODELING IN ARTERIAL HYPERTENSION (LITERATURE AND PERSONAL STUDIES’ REVIEW)
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Keywords

arterial hypertension, systemic inflammation, congenital and adaptive immunity, autophagy, vascular dysfunction, vascular remodeling

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Khaitovych , M., Bichkova, N., Potaskalova , V., & Burlaka , A. (2015). IMMUNOLOGICAL ASPECTS OF VASCULAR DYSFUNCTION AND REMODELING IN ARTERIAL HYPERTENSION (LITERATURE AND PERSONAL STUDIES’ REVIEW). Medical Science of Ukraine (MSU), 11(3-4), 108-117. Retrieved from https://msu-journal.com/index.php/journal/article/view/192

Abstract

The article provides some literature data and personal studies’ findings concerning the problem of vascular immune inflammation in arterial hypertension.

A slight elevation of arterial pressure induced by the tone increase or decrease of sympathetic and parasympathetic autonomous nervous system as well as increased activity of renin-angiotensin-aldosterone system is the cause of molecular structures’ formation related to damage-associated molecular patterns-DAMPs for cells. Micro crystals, oxygen active forms (OAF), mitochondrial DNA (mtDNA), etc are represented as DAMPs.

Effector cells of congenital immunity are activated by DAMPs through Toll-like receptors (mainlyTLR9) provoking inflammation, vascular dysfunction and remodeling. This initial inflammatory response of congenital immune system is considered to be a signal for adaptive immune system.

Аrterial hypertension contributes to T-cells differentiation into pro-inflammatory Th1. Activated Th1 cells may further a permanent raise of arterial pressure affecting vascular, renal and perivascular adipose tissue.

Autophagy (the process of intracellular components and dysfunctional organelles  degradation) plays a dual role in the inflammation control: it inhibits a basal level of inflammasome activity(being saved from depolarized or non-hermetic mitochondria, OAF and mtDNA sources, however, it helps to release IL-1ß and IL-18(and other alamines) from  cells by means of nontraditional autophago-dependent secretion at the earliest stages of physiological  activation of inflammasome in response to exogenous sources of DAMPs. 

Conclusion. Protective impact of regulatory T-lymphocytes with regard to the development of artery rigidity in arterial hypertension has been described.

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