Journal of the American Society of Hypertension
Volume 1, Issue 3 , Pages 189-199, May 2007

Increased inflammatory biomarkers in hypertensive type 2 diabetic patients: improvement after angiotensin II type 1 receptor blockade

  • Rhian M. Touyz, MD, PhD

      Affiliations

    • The Kidney Research Centre, OHRI/University of Ottawa, Ottawa, Ontario, Canada
    • Corresponding Author InformationCorresponding author: Rhian M. Touyz, MD, PhD, Kidney Research Centre, University of Ottawa/Ottawa Health Research Institute, 451 Smyth Road, Room 2513, Ottawa, Ontario, Canada, KIH 8M5. Tel: 613-562-5800; fax: 613-562-5487.
    • ,
  • Carmine Savoia, MD

      Affiliations

    • Lady Davis Research Institute, McGill University, Montreal, Quebec, Canada
    • ,
  • Ying He, MD

      Affiliations

    • The Kidney Research Centre, OHRI/University of Ottawa, Ottawa, Ontario, Canada
    • ,
  • Dierk Endemann, MD

      Affiliations

    • Lady Davis Research Institute, McGill University, Montreal, Quebec, Canada
    • ,
  • Qian Pu, MD, PhD

      Affiliations

    • Lady Davis Research Institute, McGill University, Montreal, Quebec, Canada
    • ,
  • Eun A. Ko, MD

      Affiliations

    • Lady Davis Research Institute, McGill University, Montreal, Quebec, Canada
    • ,
  • Carolina DeCiuceis, MD

      Affiliations

    • Lady Davis Research Institute, McGill University, Montreal, Quebec, Canada
    • ,
  • Augusto Montezano, PhD

      Affiliations

    • The Kidney Research Centre, OHRI/University of Ottawa, Ottawa, Ontario, Canada
    • ,
  • Ernesto L. Schiffrin, MD, PhD

      Affiliations

    • Lady Davis Research Institute, McGill University, Montreal, Quebec, Canada

Received 20 December 2006; accepted 29 January 2007.

Abstract 

Diabetes and hypertension increasingly are recognized as pro-inflammatory conditions. We tested the hypothesis that in patients with hypertension and type 2 diabetes, blood pressure (BP) reduction with an angiotensin receptor blocker (ARB), valsartan, or with a beta blocker, atenolol, is associated with a decreased inflammatory response. Normotensive subjects and hypertensive patients with type 2 diabetes (40 to 70 years of age) participated in the study. Patients (n = 28) were randomized to double-blind treatment for 1 year with valsartan (80–160 mg) or atenolol (50–100 mg) daily, added to previous therapy. Age-matched controls (n = 12) were also studied. Serum levels of cytokines (IL-6, IL-18), chemokines (MCP-1), and adhesion molecules (sICAM, sE-selectin) were measured by enzyme-linked immunosorbent assay (ELISA) as indices of systemic and vascular inflammation, before and 1 year after treatment. BP was similarly reduced by valsartan and atenolol. Glycemic control and lipid profiles were comparable in the two groups and did not change significantly with antihypertensive therapy. Serum levels of all inflammatory markers were increased in patients before treatment (by two- to four-fold vs. controls, P < .05). IL-6, IL-18, sICAM, and MCP-1 levels were reduced by valsartan (three-fold, P < .05). Only IL-18 was reduced by atenolol compared with pretreatment levels (P < .05). These data indicate that proinflammatory mediators are significantly increased in hypertensive type 2 diabetic patients and that despite similar BP lowering by valsartan and atenolol and similar glucose levels in both treated groups, global inflammatory status was improved only in the valsartan group. Our findings suggest that antihypertensive treatment, particularly with an ARB, ameliorates inflammatory processes in diabetic hypertensive patients. Such effects, which are independent of BP and glycemic control, may contribute to cardiovascular protection.

Keywords: Cytokines, chemokines, adhesion molecules, angiotensin II receptor blockers, beta blockers, glycosylated hemoglobin, blood pressure

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 This study was supported by an unrestricted grant from Novartis Pharmaceuticals Canada and by grants 44018 (to RMT) and 13570 (to ELS), as well as by a group grant to the Multidisciplinary Research Group on Hypertension, all from the Canadian Institutes for Health Research. CS and CDeC were supported in part by fellowships from the Italian Society of Hypertension. DHE was supported by a grant from the Deutsche Forschungsgemeinschaft. The authors would like to thank Mireille Kirouac, RN, for devoted follow-up of patients and blood sampling.Conflict of interest: none.

PII: S1933-1711(07)00039-3

doi:10.1016/j.jash.2007.01.009

Journal of the American Society of Hypertension
Volume 1, Issue 3 , Pages 189-199, May 2007

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