Hypertension and type 2 diabetes mellitus (DM) cause endothelial dysfunction and may result in cardiovascular disease. The aim of this study was to assess endothelial dysfunction in essential hypertensives, and normotensive and hypertensive type 2 diabetics and to evaluate the effect of telmisartan on endothelium in hypertensives. Materials and methods: Eighteen essential hypertensives (group 1), 16 type 2 diabetic hypertensives (group 2), 10 type 2 diabetic normotensives (group 3), and 10 control subjects (group 4) were included in this study. Groups 1 and 2 received 40 mg/day telmisartan for 12 weeks and were evaluated at the beginning and end. Groups 3 and 4 were evaluated once by serum nitrate (NO), vascular cell adhesion molecule-1 (VCAM-1), platelet endothelial cell adhesion molecule-1 (PECAM-1), thrombomodulin (TM), plasminogen activator inhibitor-1 (PAI-1), paraoxonase (PON1), urine microalbumin (MAU), and endothelium dependent flow mediated dilation (FMD). Results: In groups 1, 2, and 3, PAI-1 (P < 0.001, for all) and MAU (P = 0.012, P = 0.006, P = 0.004, respectively) were significantly higher than they were in group 4. In group 2, PON1 was significantly lower than it was in groups 4 and 1 (P = 0.028, P < 0.001 respectively), and NO was significantly lower than it was in groups 1, 3, and 4 (P < 0.001, for all). Brachial artery FMD was significantly lower in groups 1 and 2 than it was in group 4 and FMD in group 2 was lower than it was in group 3. After telmisartan treatment there were significant increases in PON1 in groups 1 and 2, and in TM in group 2. Conclusion: Type 2 DM and essential hypertension result in endothelial dysfunction. Telmisartan decreases blood pressure to normal ranges in hypertensives, but it has a minimal role in improvement of endothelial dysfunction.

Hypertension and type 2 diabetes mellitus (DM) cause endothelial dysfunction and may result in cardiovascular disease. The aim of this study was to assess endothelial dysfunction in essential hypertensives, and normotensive and hypertensive type 2 diabetics and to evaluate the effect of telmisartan on endothelium in hypertensives. Materials and methods: Eighteen essential hypertensives (group 1), 16 type 2 diabetic hypertensives (group 2), 10 type 2 diabetic normotensives (group 3), and 10 control subjects (group 4) were included in this study. Groups 1 and 2 received 40 mg/day telmisartan for 12 weeks and were evaluated at the beginning and end. Groups 3 and 4 were evaluated once by serum nitrate (NO), vascular cell adhesion molecule-1 (VCAM-1), platelet endothelial cell adhesion molecule-1 (PECAM-1), thrombomodulin (TM), plasminogen activator inhibitor-1 (PAI-1), paraoxonase (PON1), urine microalbumin (MAU), and endothelium dependent flow mediated dilation (FMD). Results: In groups 1, 2, and 3, PAI-1 (P < 0.001, for all) and MAU (P = 0.012, P = 0.006, P = 0.004, respectively) were significantly higher than they were in group 4. In group 2, PON1 was significantly lower than it was in groups 4 and 1 (P = 0.028, P < 0.001 respectively), and NO was significantly lower than it was in groups 1, 3, and 4 (P < 0.001, for all). Brachial artery FMD was significantly lower in groups 1 and 2 than it was in group 4 and FMD in group 2 was lower than it was in group 3. After telmisartan treatment there were significant increases in PON1 in groups 1 and 2, and in TM in group 2. Conclusion: Type 2 DM and essential hypertension result in endothelial dysfunction. Telmisartan decreases blood pressure to normal ranges in hypertensives, but it has a minimal role in improvement of endothelial dysfunction.