Open AccessHypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus
Author(s) -
McClung Daniel M.,
Kalusche William J.,
Jones Katie E.,
Ryan Michael J.,
Taylor Erin B.
Publication year - 2021
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.14734
Subject(s) - pristane , medicine , endothelial dysfunction , autoantibody , immunology , systemic lupus erythematosus , rheumatoid arthritis , autoimmunity , immune system , lupus erythematosus , autoimmune disease , arthritis , endocrinology , antibody , disease , chemistry , hydrocarbon , organic chemistry
Autoimmune diseases such as psoriasis, rheumatoid arthritis, and systemic lupus erythematosus (SLE) have high rates of hypertension and cardiovascular disease. Systemic lupus erythematosus is a prototypic autoimmune disorder that primarily affects women of childbearing age and is associated with a loss of self‐tolerance, autoreactive B and T lymphocytes, and the production of autoantibodies, especially to nuclear components. In this study, we hypothesized that the pristane‐inducible model of SLE would develop hypertension and vascular dysfunction as the disease progressed. To test this hypothesis, female C57BL/6 mice were administered PBS or pristane. Seven months after pristane administration, mice developed various autoantibodies, including anti‐dsDNA IgG, anti‐ssDNA IgG, and anti‐nRNP IgG, as well as hypergammaglobulinemia. Several other immunological changes, including increased circulating neutrophils and increased CD4 − CD8 − (double negative) thymocytes were also detected. Mean arterial pressure (MAP) was elevated in pristane‐treated mice when compared to PBS‐treated mice. In addition, second‐order mesenteric arteries from pristine‐treated mice had impaired relaxation to the endothelium‐dependent vasodilator acetylcholine compared to PBS‐treated mice. These data suggest that the immune system dysfunction present in the pristane model of lupus contributes to the development of hypertension and vascular dysfunction.