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- Title
Early markers of inflammation in a high angiotensin II state-results of studies in Bartter’s/Gitelman’s syndromes.
- Authors
Davis, Paul A.; Mussap, Michele; Pagnin, Elisa; Bertipaglia, Lara; Savica, Vincenzo; Semplicini, Andrea; Calò, Lorenzo A.
- Abstract
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-α (TNF-α ) using immunonephelometric and ELISA-based assays. Results. The study demonstrated that all markers of inflammation except TNF-α , 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-α 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.
- Publication
Nephrology Dialysis Transplantation, 2006, Vol 21, Issue 6, p1697
- ISSN
0931-0509
- Publication type
Article
- DOI
10.1093/ndt/gfl112