Mechanisms of hypertension in autoimmune rheumatic diseases

Abstract

Patients with autoimmune rheumatic diseases including rheumatoid arthritis and systemic lupus erythematosus have an increased prevalence of hypertension. There is now a large body of evidence showing that the immune system is a key mediator in both human primary hypertension and experimental models. Many of the proposed immunological mechanisms leading to primary hypertension are paralleled in autoimmune rheumatic disorders. Therefore, examining the link between autoimmunity and hypertension can be informative for understanding primary hypertension. This review examines the prevalent hypertension, the immune mediators that contribute to the prevalent hypertension and their impact on renal function and how the risk of hypertension is potentially influenced by common hormonal changes that are associated with autoimmune rheumatic diseases. LINKED ARTICLES: This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc.

Figure 1

Immune system dysfunction in autoimmunity contributes to the development of hypertension. The crosstalk between the innate and adaptive immune systems leads to a chronic inflammatory state that affects the kidney, vasculature, and CNS, all promoting the development of autoimmune‐associated hypertension

Figure 2

The role of the immune system in renal haemodynamic function. Autoantibodies and immune complexes, renal leukocytes, and inflammatory cytokines promote specific changes in the kidney leading to altered renal haemodynamics, impaired pressure natriuresis, and the development of hypertension.