Increased inflammatory biomarkers in hypertensive type 2 diabetic patients: improvement after angiotensin II type 1 receptor blockade |
| |
| Institution: | 1. The Kidney Research Centre, OHRI/University of Ottawa, Ottawa, Ontario, Canada;2. Lady Davis Research Institute, McGill University, Montreal, Quebec, Canada;1. Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy;2. Center for Atherosclerosis, Policlinico Tor Vergata, Rome, Italy;3. Unit of Biostatistics, IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy;4. Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, Rome, Italy;5. Department of Biopathology and Diagnostic Imaging, University of Rome Tor Vergata, Italy;1. General Hospital of Chinese People’s Liberation Army, Beijing 100853, PR China;2. Beijing Institute of Basic Medical Sciences, Beijing 100850, PR China;3. Affiliated Hospital of General Hospital of Chinese People’s Liberation Army, Beijing 100048, PR China;1. Laboratório de Polimorfismos Genéticos, Universidade Federal de Santa Catarina LAPOGE/ (UFSC), Florianópolis, SC, Brasil;2. Hospital das Clínicas, Faculdade de Medicina, Universidade do Estado de São Paulo (HC-FMUSP), São Paulo, SP, Brasil;3. Serviço de Reumatologia, Hospital Universitário, Universidade Federal de Santa Catarina (HU-UFSC), Florianópolis, SC, Brasil;1. School of Management and Economics, University of Electronic Science and Technology, 610054 Chengdu, PR China;2. School of Finance, Southwestern University of Finance and Economics, 610074 Chengdu, PR China;3. College of Science, Ningbo University of Technology, 315211 Ningbo, PR China;4. Department of Physics, University of Fribourg, Chemin du Musée 3, CH-1700 Fribourg, Switzerland;1. School of Software, Dalian University of Technology, Dalian 116621, China;2. School of Information Science and Engineering, Ludong University, Yantai 264025, China;3. Computational Social Science Lab, School of Innovation Experiment, Dalian University of Technology, Dalian 116024, China;1. ETH Zurich, Department of Biosystems Science and Engineering, Mattenstrasse 26, 4058 Basel, Switzerland;2. Swiss Institute of Bioinformatics, Switzerland |
| |
| 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: | |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
