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Am J Physiol Regul Integr Comp Physiol 296: R1258-R1267, 2009. First published January 21, 2009; doi:10.1152/ajpregu.90864.2008
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REVIEW

WATER AND ELECTROLYTE HOMEOSTASIS

Young Investigator Award Lecture of the APS Water and Electrolyte Homeostasis Section, 2008: The pathophysiology of hypertension in systemic lupus erythematosus

Michael J. Ryan

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi

Submitted 27 October 2008 ; accepted in final form 15 January 2009

ABSTRACT

Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder that predominantly affects women during their reproductive years. Although SLE can affect any organ system, the kidneys are prominently involved in the form of immune complex glomerulonephritis. In addition, in women with SLE, risk for the development of cardiovascular disease is dramatically increased. Hypertension is a major risk factor for cardiovascular disease and is highly prevalent in women with SLE. Nevertheless, there has been little exploration of the pathophysiological mechanisms that promote SLE hypertension. This review discusses the role of several mechanisms, with an emphasis on the kidney, in SLE hypertension. These mechanisms include the renin-angiotensin system, endothelin, oxidative stress, sex steroids, metabolic changes, peroxisome proliferator-activated receptor-{gamma}, and, perhaps most importantly, chronic inflammation and cytokines. Growing evidence suggests a link between chronic inflammation and hypertension. Therefore, elucidation of mechanisms that promote SLE hypertension may be of significant value not only for patients with SLE, but also for a better understanding of the basis for essential hypertension.

renal; inflammation



Address for reprint requests and other correspondence: M. J. Ryan, Physiology & Biophysics, Univ. of Mississippi Medical Center, Jackson, MS 39216 (e-mail: mjryan{at}physiology.umsmed.edu)







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