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Review
. 2019 Mar;26(2):122-130.
doi: 10.1053/j.ackd.2019.03.001.

Inflammation, Immunity, and Oxidative Stress in Hypertension-Partners in Crime?

Ian R Barrows  1 , Ali Ramezani  1 , Dominic S Raj  2
Affiliations
Review

Inflammation, Immunity, and Oxidative Stress in Hypertension-Partners in Crime?

Ian R Barrows et al. Adv Chronic Kidney Dis. 2019 Mar.

Abstract

Hypertension is considered as the most common risk factor for cardiovascular disease. Inflammatory processes link hypertension and cardiovascular disease, and participate in their pathophysiology. In recent years, there has been an increase in research focused on unraveling the role of inflammation and immune activation in development and maintenance of hypertension. Although inflammation is known to be associated with hypertension, whether inflammation is a cause or effect of hypertension remains to be elucidated. This review describes the recent studies that link inflammation and hypertension and demonstrate the involvement of oxidative stress and endothelial dysfunction-two of the key processes in the development of hypertension. Etiology of hypertension, including novel immune cell subtypes, cytokines, toll-like receptors, inflammasomes, and gut microbiome, found to be associated with inflammation and hypertension are summarized and discussed. Most recent findings in this field are presented with special emphasis on potential of anti-inflammatory drugs and statins for treatment of hypertension.

Keywords: Anti-inflammatory drugs; Hypertension; Immune activation; Inflammation; Oxidative stress.

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Figures

Figure 1.
Figure 1.. Innate and adaptive immune cells that play a role in hypertension.
Innate immune cells such as monocytes, macrophages, and dendritic cells (DC) inhibit or promote hypertension by producing various cytokines and reactive oxygen species (ROS). Monocytes and dentric cells (DC) also contain the NLRP3 inflammasome which also plays an important role in hypertension. Adaptive immune cells such as the B cells, CD4+ T cells (Treg, Th17, and Th1 cells), and CD8+ T cells also produce cytokines that inhibit or promote hypertension.
Figure 2.
Figure 2.. Immune cell activation and inflammation as critical mediators of hypertension.
Activation of central nervous system by hypertensive stimuli such as angiotensin II (Ang II), high salt intake, reactive oxygen species (ROS) and chronic stress will lead to an increase in sympathetic outflow, which causes a modest elevation in blood pressure (pre-hypertension). Elevation of pressure will lead to increase ROS production in the kidney and vasculature, and formation of neoantigens from endogenous proteins. These neoantigens are presented to T cells by DCs, causing T cell activation and cytokine production, including IL17. These cytokine productions will promote inflammation and oxidative stress in kidney and vascular smooth muscle leading to sodium retention, vasoconstriction and overt-hypertension.
Figure 3.
Figure 3.. Some of the factors that play a key role in control of blood pressure by affecting the basic equation blood pressure = cardiac output (CO) × peripheral resistance (PR).
Elevation in blood pressure is medicated by the collective contribution of a number of genetic, environmental (including diet) and physiological factors. Both excess sodium intake and renal sodium retention would presumably work primarily on increasing fluid volume and cardiac output. Various hormonal mediators, including angiotensin II, nitric oxide and endothelin may initiate the increased peripheral resistance.
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