Immunological Aspects of Essential Hypertension

Abstract

According to modern concept of the etiopathogenesis of essential hypertension, immune cells play an important role in its development. Mediators produced by immunocompetent cells participate in the initiation and maintenance of chronic systemic inflammation and promote the development of vascular remodeling which is an important part of the pathogenesis of the disease and target organ damage. The immune mechanisms underlying blood pressure elevation include the activation of innate and adaptive immune cells. Endothelial damage triggers an inflammatory cascade, causing migration of the immune cells to the inflammatory site, mediated by chemokines and adhesion molecules. Macrophage infiltration of perivascular tissue contributes to impaired vasodilation and damage to target organs due to the production of active forms of oxygen. Angiotensin II also causes T cell infiltration of perivascular adipose tissue and adventitia and an increased production of tumor necrosis factor alpha and interferon gamma. In addition, T lymphocytes express the mineralocorticoid receptor involved in the development of systemic hypertension. An important role in the progression of hypertension belongs to interleukin-17, which is involved in blood pressure elevation and vascular remodeling. The review also contains data on the effect of gut microbiota on the regulation of blood pressure and the development of hypertension.

Analysis of changes in cytokine concentrations and neutrophil activity in patients with essential arterial hypertension depending on the affected target organs against the background of antihypertensive therapy

“…Так, при гипертрофии миокарда левого желудочка и при бессимптомном атеросклерозе сосудов снижается фагоцитарная активность нейтрофилов периферической крови и повышается их кислород-зависимая активность, тогда как при хронической болезни почек фагоцитарная активность нейтрофилов не изменена. Повышение показателей НСТ-теста, наблюдаемое во всех изученных группах больных артериальной гипертонией, отражает генерацию активных форм кислорода, что приводит к развитию «окислительного стресса» в тканях органа-мишени: сосуды -атеросклеротическое поражение, почки -развитие хронической болезни почек, сердце -гипертрофия миокарда [17].…”

Relationship between immunological alterations, hypoxia and inflammation in arterial hypertension combined with metabolic syndrome

“…Previously, it was shown that level of fibrinogen, C-reactive protein (CRP) and neopterin was increased in inflammatory events, which serve as sensitive markers for inflammation and necrosis. Their rise in the serum higher than reference values correlates with increased risk of complications in cardiovascular diseases [9,10].…”

Role of immunological disorders, endothelial dysfunction and hemostatic disorders in the genesis of arterial hypertension in the metabolic syndrome

“…Th1-подтип лимфоцитов генерирует выработку TNFα, IL-2, IFNγ; Th2-подтип продуцирует IL-4, IL-5, IL-10, IL-13, ингибирует клеточно-опосредованный иммунитет и стимулирует В-лимфоциты. [27,40].…”