NDT Advance Access originally published online on March 30, 2006
Nephrology Dialysis Transplantation 2006 21(6):1697-1701; doi:10.1093/ndt/gfl112
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Short Communication
Early markers of inflammation in a high angiotensin II state—results of studies in Bartter's/Gitelman's syndromes
1 Department of Nutrition, University of California, Davis, 2 Department of Laboratory Medicine, 3 Department of Clinical and Experimental Medicine, Clinica Medica 4, University of Padova and 4 Division of Nephrology, University of Messina, Italy
Correspondence and offprint requests to: Lorenzo A. Calò, MD, PhD, Department of Clinical and Experimental Medicine, Clinica Medica 4, University of Padova, Via Giustiniani, 2, 35128 Padova, Italy. Email: renzcalo{at}unipd.it
Background. Inflammation has been increasingly recognized as playing a critical role in hypertension and atherosclerosis as reflected by overexpression and increased production of a variety of pro-inflammatory mediators. As angiotensin II (Ang II) also plays a major role in these diseases, the relationship between inflammation and Ang II has drawn increasing scrutiny. This study explores Ang II effects in Bartter's and Gitelman's syndromes (BS/GS) which do not develop hypertension and related cardiovascular remodelling and atherosclerosis, in spite of high Ang II levels and activation of the renin–angiotensin–aldosterone system while the NO system is up-regulated.
Methods. We evaluated the plasma levels of inflammation-associated markers, C-reactive protein (CRP), serum amyloid A (SAA), vascular cell adhesion molecules (VCAM) and intercellular adhesion molecules (ICAM), and the inflammation-related cytokines interleukin-6 (IL-6) and tumour necrosis factor-
(TNF-) using immunonephelometric and ELISA-based assays.
Results. The study demonstrated that all markers of inflammation except TNF-, were unchanged in BS/GS (2.51±0.62 mg/l in BS/GS vs 1.7±0.6 in controls for CRP; 4.56±1.09 mg/l in BS/GS vs 4.51±1.0 for SAA; 1.84±0.27 ng/l in BS/GS vs 2.1±0.3 for IL-6; 449±83 ng/ml in BS/GS vs 410±92 for VCAM and 234±26 ng/ml in BS/GS vs 185±22 for ICAM), while TNF- was increased (10.5±2.03 vs 3.68±0.2, P = 0.0001).
Conclusions. The results of this study stress the critical role played by Ang II in controlling vascular biology including inflammation-related processes as well as highlighting the utility of BS/GS in investigating these pathways.
Keywords: angiotensin II; atherosclerosis; Bartter's syndrome; Gitelman's syndrome; hypertension; inflammation
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  L. A. Calo, M. Puato, S. Schiavo, M. Zanardo, C. Tirrito, E. Pagnin, G. Balbi, P. A. Davis, P. Palatini, and P. Pauletto Absence of vascular remodelling in a high angiotensin-II state (Bartter's and Gitelman's syndromes): implications for angiotensin II signalling pathways Nephrol. Dial. Transplant., September 1, 2008; 23(9): 2804 - 2809. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. I. Ager, J. Neo, and C. Christophi The renin-angiotensin system and malignancy Carcinogenesis, September 1, 2008; 29(9): 1675 - 1684. [Abstract] [Full Text] [PDF]
|
|