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(Hypertension. 2007;50:829.)
© 2007 American Heart Association, Inc.

Hypertension Case Report

Autoimmune Hypertensive Syndrome

David C. Kem; Xichun Yu; Eugene Patterson; Shijun Huang; Stavros Stavrakis; Bela Szabo; Leann Olansky; Jon McCauley; Madeleine W. Cunningham

From the Departments of Medicine (D.C.K., X.Y., E.P., S.H., S.S., B.S., L.O.), Cell Biology (E.P.), Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and VA Medical Center, Oklahoma City; and McAlester Clinic (J.M.), McAlester, Okla. Current address (L.O.): The Cleveland Clinic, Ohio.

Correspondence to David C. Kem, WP-1345, 920 Stanton Young Blvd, Oklahoma City, OK 73104. E-mail david-kem@ouhsc.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Intravenous infusion of epinephrine or norepinephrine produces hypertension and symptoms similar to a pheochromocytoma.^1,2 The sequelae are predictable on the basis of continuous infusion of agonists that activate ß and adrenergic receptors (ARs). These monoamine agonists, however, are not the only means by which ß-ARs can be activated. Activating autoantibodies (AAs) directed toward the ß₁AR and/or the ß₂AR have been demonstrated in some patients with idiopathic dilated cardiomyopathy,^3–5 Chagas’ disease,^6,7 and other forms of cardiomyopathy.^8,9 Several studies have demonstrated that these antibodies possess the ability to activate the intrinsic ßAR signal transduction system; however, these studies have focused only on the possible relationship of the AAßAR agonist effects on cardiomyopathy. Because ß-agonist excess also produces changes in systemic blood pressure, one would expect the presence of AAßAR to produce a phenotype including some features observed in patients with an epinephrine-only secretory neuroendocrine tumor. Isolated studies have reported the concurrence of activating autoantibodies to the ₁AR^10,11 or to the angiotensin receptor (AT1)^12,13 in a few patients with associated hypertension.

Herein, we present a hypertensive patient with no clinical evidence for a pheochromocytoma secreting excess catecholamine(s). However, in year 2000, there was conclusive evidence for anti-ßAR autoantibodies, which in vitro activate the ßAR signal transduction system independent of the intrinsic hormone-mediated system. Subsequent study in sera obtained in 2006 confirmed these data. These autoantibodies, as a result of their peptide sequence specificity, do not activate the -adrenergic transduction system, as would norepinephrine or epinephrine at higher dosages. The evidence that . . . [Full Text of this Article]

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