Effects of 12-Month Valsartan Therapy on Glycation and Oxidative Stress Markers in Type 2 Diabetic Subjects With Hypertension

Abstract

SUMMARYAlthough it has been reported that angiotensin II receptor blockers inhibited the formation and accumulation of advanced glycation endproducts (AGEs) in vitro and in vivo, whether they can do so clinically is not clear. We investigated the effects of 12-month valsartan therapy on various markers of inflammation, glycation, and oxidation in type 2 diabetic subjects with hypertension.We started 40 mg/day valsartan treatment in 15 type 2 diabetic patients with hypertension. In 6 patients, the dose of valsartan was increased to 80 mg/day after 6 months and maintained until 12 months. Metabolic parameters including BMI and serum high molecular weight (HMW)-adiponectin, high-sensitivity C-reactive protein (hs-CRP) as an inflammation marker, AGEs, paraoxonase activity, platelet-activating factor (PAF)-acetylhydrolase activity, and urine 8-isoprostane levels were measured at baseline and after 6 and 12 months of treatment. Urine microalbumin level and carotid artery intimamedia thickness (IMT) were also measured.Even after valsartan therapy, the blood pressure levels of the patients were not decreased significantly. Serum AGEs and urine 8-isoprostane levels decreased at both 6 and 12 months (P < 0.05 for both), although other metabolic and oxidative markers were unchanged. Though urine microalbumin levels tended to be decreased after 6 and 12 months of valsartan treatment, the changes were not significant. Mean IMT at 12 months was not changed from the baseline value. In conclusion, the findings suggest that treatment with valsartan, even at a low dose, may ameliorate some glycation and oxidative stress markers independently of an effect on blood pressure in hypertensive type 2 diabetic subjects. (Int Heart J 2008; 49: 681-689)

Effect of Nisoldipine and Olmesartan on Endothelium‐Dependent Vasodilation in Essential Hypertensive Patients

“…Consistent with the literature [29,30], we found increased levels of 8-isoPGF2α, a marker of oxidative stress, in essential hypertensive patients. However, our treatment with nisoldipine or olmesartan failed to cause any apparent reduction in 8-isoPGF2α levels in the patients, indicating that nisoldipine or olmesartan did not improve endothelial function by militating against oxidative stress in hypertensive subjects.…”

Intermediate Monocytes Lead to Enhanced Myocardial Remodelling in STEMI Patients With Diabetes

“…19,20) The subsets show high activation and inflammatory potential by selective upregulating of genes (AIF1 and TGFB1) linked to the inflammatory processes and display the ability to produce reactive oxygen species. 21,22) Therefore, the biological behaviour of these monocytes in AMI patients with diabetes should be determined because these patients are associated with increased immediate and long-term systemic inflammation, [23][24][25] especially in small and large blood vessels.…”

Targeting advanced glycation endproducts and mitochondrial dysfunction in cardiovascular disease

“…Focuses were trained upon differing endpoint analysis not always related directly to CVD. Further studies highlighted reduction in AGEs serum levels with treatment [57]. But confliction was presented in larger cohorts with no reduction in AGE accumulation [58].…”