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      Mechanisms of hypertension in autoimmune rheumatic diseases

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          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.

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          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

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          Most cited references176

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          The complex role of estrogens in inflammation.

          Rainer H. Straub (2007)
          There is still an unresolved paradox with respect to the immunomodulating role of estrogens. On one side, we recognize inhibition of bone resorption and suppression of inflammation in several animal models of chronic inflammatory diseases. On the other hand, we realize the immunosupportive role of estrogens in trauma/sepsis and the proinflammatory effects in some chronic autoimmune diseases in humans. This review examines possible causes for this paradox. This review delineates how the effects of estrogens are dependent on criteria such as: 1) the immune stimulus (foreign antigens or autoantigens) and subsequent antigen-specific immune responses (e.g., T cell inhibited by estrogens vs. activation of B cell); 2) the cell types involved during different phases of the disease; 3) the target organ with its specific microenvironment; 4) timing of 17beta-estradiol administration in relation to the disease course (and the reproductive status of a woman); 5) the concentration of estrogens; 6) the variability in expression of estrogen receptor alpha and beta depending on the microenvironment and the cell type; and 7) intracellular metabolism of estrogens leading to important biologically active metabolites with quite different anti- and proinflammatory function. Also mentioned are systemic supersystems such as the hypothalamic-pituitary-adrenal axis, the sensory nervous system, and the sympathetic nervous system and how they are influenced by estrogens. This review reinforces the concept that estrogens have antiinflammatory but also proinflammatory roles depending on above-mentioned criteria. It also explains that a uniform concept as to the action of estrogens cannot be found for all inflammatory diseases due to the enormous variable responses of immune and repair systems.
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            Age-specific incidence rates of myocardial infarction and angina in women with systemic lupus erythematosus: comparison with the Framingham Study.

            S Manzi, E Meilahn, J. E Rairie … (1997)
            The authors ascertained cardiovascular events (myocardial infarction and angina pectoris) in 498 women with systemic lupus erythematosus seen at the University of Pittsburgh Medical Center from 1980 to 1993 (3,522 person-years). Subjects were stratified by age, and cardiovascular event incidence rates were determined. The authors compared these rates with cardiovascular event rates were determined. The authors compared these rates with cardiovascular event rates occurring over the same time period in 2,208 women of similar age participating in the Framingham Offspring Study (17,519 person-years). Age-specific rate ratios were computed to determine whether the cardiovascular events in the lupus cohort were greater than expected. The risk factors associated with cardiovascular events in women with lupus were determined. There were 33 first events (11 myocardial infarction, 10 angina pectoris, and 12 both angina pectoris and myocardial infarction) after the diagnosis of lupus: two thirds were under the age of 55 years at the time of event. Women with lupus in the 35- to 44-year age group were over 50 times more likely to have a myocardial infarction than were women of similar age in the Framingham Offspring Study (rate ratio = 52.43, 95% confidence interval 21.6-98.5). Older age at lupus diagnosis, longer lupus disease duration, longer duration of corticosteroid use, hypercholesterolemia, and postmenopausal status were more common in the women with lupus who had a cardiovascular event than in those who did not have an event. Premature cardiovascular disease is much more common in young premenopausal women with lupus than in a population sample. With the increased life expectancy of lupus patients due to improved therapy, cardiovascular disease has emerged as a significant threat to the health of these women. The impact of this problem has been underrecognized, with little focus placed on aggressive management of hypercholesterolemia and other possible risk factors.
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              Combined oral contraceptives in women with systemic lupus erythematosus.

              Michelle Petri, Mimi Y. Kim, Kenneth Kalunian … (2005)
              Oral contraceptives are rarely prescribed for women with systemic lupus erythematosus, because of concern about potential negative side effects. In this double-blind, randomized, noninferiority trial, we prospectively evaluated the effect of oral contraceptives on lupus activity in premenopausal women with systemic lupus erythematosus. A total of 183 women with inactive (76 percent) or stable active (24 percent) systemic lupus erythematosus at 15 U.S. sites were randomly assigned to receive either oral contraceptives (triphasic ethinyl estradiol at a dose of 35 microg plus norethindrone at a dose of 0.5 to 1 mg for 12 cycles of 28 days each; 91 women) or placebo (92 women) and were evaluated at months 1, 2, 3, 6, 9, and 12. Subjects were excluded if they had moderate or high levels of anticardiolipin antibodies, lupus anticoagulant, or a history of thrombosis. The primary end point, a severe lupus flare, occurred in 7 of 91 subjects receiving oral contraceptives (7.7 percent) as compared with 7 of 92 subjects receiving placebo (7.6 percent). The 12-month rates of severe flare were similar: 0.084 for the group receiving oral contraceptives and 0.087 for the placebo group (P=0.95; upper limit of the one-sided 95 percent confidence interval for this difference, 0.069, which is within the prespecified 9 percent margin for noninferiority). Rates of mild or moderate flares were 1.40 flares per person-year for subjects receiving oral contraceptives and 1.44 flares per person-year for subjects receiving placebo (relative risk, 0.98; P=0.86). In the group that was randomized to receive oral contraceptives, there was one deep venous thrombosis and one clotted graft; in the placebo group, there was one deep venous thrombosis, one ocular thrombosis, one superficial thrombophlebitis, and one death (after cessation of the trial). Our study indicates that oral contraceptives do not increase the risk of flare among women with systemic lupus erythematosus whose disease is stable. Copyright 2005 Massachusetts Medical Society.
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                Author and article information

                Contributors
                Michael J. Ryan:
                ORCID: https://orcid.org/0000-0002-5679-6031
                mjryan@umc.edu
                Journal
                Journal ID (nlm-ta): Br J Pharmacol
                Journal ID (iso-abbrev): Br. J. Pharmacol
                Journal ID (doi): 10.1111/(ISSN)1476-5381
                Journal ID (publisher-id): BPH
                Title: British Journal of Pharmacology
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0007-1188
                ISSN (Electronic): 1476-5381
                Publication date (Electronic): 18 March 2019
                Publication date (Print): June 2019
                Publication date PMC-release: 18 March 2019
                Volume: 176
                Issue: 12 , Themed Section: Immune Targets in Hypertension. Guest Editors: Antony Vinh, Grant R. Drummond and Christopher G. Sobey ( doiID: 10.1111/bph.v176.12 )
                Pages: 1897-1913
                Affiliations
                [ 1 ] Department of Physiology and Biophysics University of Mississippi Medical Center Jackson Mississippi USA
                [ 2 ] G.V. (Sonny) Montgomery Veterans Affairs Medical Center Jackson Mississippi USA
                Author notes
                [*] [* ] Correspondence

                Michael J. Ryan, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216‐4505, USA.

                Email: mjryan@ 123456umc.edu

                Author information
                http://orcid.org/0000-0003-0122-0833
                http://orcid.org/0000-0002-1460-9787
                http://orcid.org/0000-0002-8565-1157
                https://orcid.org/0000-0002-5679-6031
                Article
                Publisher ID: BPH14604 Other ID: 2018-BJP-0707-RCT-G.R2
                DOI: 10.1111/bph.14604
                PMC ID: 6534791
                PubMed ID: 30714094
                SO-VID: 3c2cdd09-3c7e-4180-8db2-3247c3bb0c81
                Copyright © © 2019 The Authors. British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                Date received : 13 June 2018
                Date revision received : 12 December 2018
                Date accepted : 07 January 2019
                Page count
                Figures: 2, Tables: 0, Pages: 17, Words: 8847
                Funding
                Funded by: National Heart, Lung, and Blood Institute
                Award ID: F32HL137393
                Award ID: PO1HL051971
                Award ID: T32HL105324‐05
                Award ID: 5U54GM115428
                Award ID: P20GM104357
                Funded by: National Institute of General Medical Sciences
                Award ID: 5U54GM115428
                Award ID: P20GM104357
                Funded by: U.S. Department of Veterans Affairs
                Award ID: BX002604‐01A2
                Funded by: American Heart Association
                Award ID: 17POST33410862
                Categories
                Subject: Review Article
                Subject: Themed Section: Review Articles
                Custom metadata
                source-schema-version-number 2.0
                component-id bph14604
                cover-date June 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.3 mode:remove_FC converted:25.05.2019

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine

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