Published online before print January 29, 2007, doi: 10.1161/01.HYP.0000257805.64783.d9
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(Hypertension. 2007;49:e18.)
© 2007 American Heart Association, Inc.
Letters to the Editor |
Interleukin-6 Antagonists for the Management of Hypertension
Department of Family Medicine, University of Illinois at Chicago, Chicago, Ill
I read with great interest the recent article published by Luther et al1 in the December 2006 issue of Hypertension, which focused on how angiotensin II induces interleukin (IL)-6 in humans. The authors suggest that angiotensin II performs this function through a mineralocorticoid receptor–dependent mechanism.
I would like to suggest the possible future role of IL-6 antagonists in the control and treatment of recalcitrant hypertension. Abnormal IL-6 levels have been noted in almost all types of inflammatory disorders. Abnormal IL-6 production has also been noted in acute coronary syndromes2 and a number of malignancies, such as multiple myeloma. It is widely believed that IL-6 may have a major role to play in the pathogenesis of almost all inflammatory disorders in the body.
Manfredini et al3 reported the development of an IL-6 peptide antagonist that was shown to reduce IL-6 activity in vitro. Another molecule that is currently being studied is tocilizumab. Tocilizumab is an antihuman IL-6 receptor antibody of the IgG1 subclass currently used primarily in the treatment of rheumatoid arthritis. It binds to both the soluble and the membrane-bound forms of IL-6 receptors, thus markedly reducing binding of IL-6 to its receptors and, thus, reducing its proinflammatory function.4 Molecules such as tocilizumab have shown considerable promise as IL-6 antagonists and may play a vital role in management of recalcitrant hypertension in the near future.
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Acknowledgments |
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Disclosures
None.
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References |
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 Top References |
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1. Luther JM, Gainer JV, Murphey LJ, Yu C, Vaughan DE, Morrow JD, and Brown NJ. Angiotensin II induces IL-6 in humans through a mineralocorticoid receptor-dependent mechanism. Hypertension. 2006; 48: 1050–1057.
2. Schieffer B, Schieffer E, Hilfiker-Kleiner D, Hilfiker A, Kovanen PT, Kaartinen M, Nussberger J, Harringer W, Drexler H. Expression of angiotensin II and IL 6 in human coronary atherosclerotic plaques: potential implications for inflammation and plaque instability. Circulation. 2000; 101: 1372–1378.
3. Manfredini R, Tenedini E, Siena M, Tagliafico E, Montanari M, Grande A, Zanocco-Marani T, Poligani C, Zini R, Gemelli C, Bergamaschi A, Vignudelli T, De Rienzo F, De Benedetti PG, Menziani MC, Ferrari S. Development of an IL-6 antagonist peptide that induces apoptosis in 7TD1 cells. Peptides. 2003; 24: 1207–1220.[CrossRef][Medline] [Order article via Infotrieve]
4. Maini RN, Taylor PC, Szechinski J, Pavelka K, Broll J, Balint G, Emery P, Raemen F, Petersen J, Smolen J, Thomson D, Kishimoto T, and CHARISMA Study Group. Double-blind randomized controlled clinical trial of the IL-6 receptor antagonist, tocilizumab, in european patients with rheumatoid arthritis who had an incomplete response to methotrexate. Arthritis Rheum. 2006; 54: 2817–2829.[CrossRef][Medline] [Order article via Infotrieve]
This article has been cited by other articles:
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  J. M. Luther and N. J. Brown Response to Interleukin-6 Antagonists for the Management of Hypertension Hypertension, March 1, 2007; 49(3): e19 - e19. [Full Text] [PDF]
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