10.1 Linkage Between Inflammation and Hypertension in Humans: Evidence from Studies on Bartter’s/Gitelman’s Syndromes
Introduction: Inflammation has been increasingly recognised as playing a critical role in hypertension and atherosclerosis as reflected by overexpression and increased production of a variety of pro-inflammatory mediators. The relationship between inflammation, Angiotensin II (Ang II) II and its signaling has drawn increasing scrutiny but few data are available in humans. Patients with Bartter’s/Gitelman’s syndromes (BS/GS) do not develop hypertension and related cardiovascular remodelling and atherosclerosis despite high Ang II levels, therefore making these syndromes a useful human model for investigating mechanisms involved in the regulation of vascular tone and remodelling. This study explores in BS/GS the inflammation status through the evaluation of some factors included in Ang II signaling involved in inflammation such as Extracellular signal-regulated kinase (ERK), IkB (inhibitory subunit of NFkB) and p66shc, an adaptor protein involved in the response to oxidative stress.
Methods: We evaluated in mononuclear cells the protein levels of Phosphorylated ERK, IkB using Western Blots and p66shc gene expression using RT-PCR.
Results: The study demonstrated that phosphorylated (P)-ERK/ERK ratio and p66shc in patients with BS/GS were unchanged compared to Controls (9.8 ± 9.3 vs 8.4±12.8 and 0.65±0.08 vs 0.64 ±0.09 respectively) while IkB was increased (1.75±0.69 vs 0.67 ±0.31 respectively, p<0,05).
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Calò, L., Pagnin, E., Schiavo, S. et al. 10.1 Linkage Between Inflammation and Hypertension in Humans: Evidence from Studies on Bartter’s/Gitelman’s Syndromes. High Blood Press Cardiovasc Prev 14, 145 (2007). https://doi.org/10.2165/00151642-200714030-00167