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

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. (C) 2007 American Society of Hypertension. All rights reserved.