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ADMA and oxidative stress may relate to the progression of renal disease: rationale and design of the VIVALDI study.
Vasc Med. 2005 Jul; 10 Suppl 1:S97-102.VM

Abstract

The renin angiotensin system has been shown to be involved in the pathogenesis of vascular and renal sequelae of diabetes mellitus. In type 2 diabetes mellitus, angiotensin receptor blockers have been shown to exert clinical benefit by reducing the progression of diabetic nephropathy. They also improve endothelium-mediated vascular function. The latter effect is partly due to the reduction of angiotensin II-associated oxidative stress. Moreover, small clinical studies have shown that treatment with angiotensin receptor blockers also reduces the circulating levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthase. In the VIVALDI trial, the ability of the angiotensin receptor blocker telmisartan to reduce the progression of diabetic nephropathy (associated with proteinuria) in comparison with valsartan in more than 800 patients with type 2 diabetes during 1 year of treatment is being studied. In order to gain more detailed insight into the potential pathomechanisms associated with this effect, further end-points have been defined. Among these are the circulating levels of ADMA and the urinary excretion rate of 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha). The former is an endogenous inhibitor of NO-mediated vascular function(s) and a prospectively determined marker of major cardiovascular events and mortality; the latter is a lipid peroxidation product resulting from the nonenzymatic peroxidation of arachidonic acid, which exerts detrimental vascular effects similar to those of thromboxane A2. Urinary 8-iso-PGF2alpha has been shown in clinical studies to be an independent marker of cardiovascular disease. Highlighting the effects of telmisartan on ADMA and 8-iso-PGF levels in such a large cohort of diabetic patients will enhance our understanding of the roles of dysfunctional NO metabolism and redox mechanisms in the pathogenesis of end-organ damage and its prevention by pharmacotherapy with angiotensin receptor blockers.

Authors+Show Affiliations

Institute of Experimental and Clinical Pharmacology, University Hospital Hamburg-Eppendorf, Germany. boeger@uke.uni-hamburg.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

16444875

Citation

Böger, Rainer H., et al. "ADMA and Oxidative Stress May Relate to the Progression of Renal Disease: Rationale and Design of the VIVALDI Study." Vascular Medicine (London, England), vol. 10 Suppl 1, 2005, pp. S97-102.
Böger RH, Schwedhelm E, Maas R, et al. ADMA and oxidative stress may relate to the progression of renal disease: rationale and design of the VIVALDI study. Vasc Med. 2005;10 Suppl 1:S97-102.
Böger, R. H., Schwedhelm, E., Maas, R., Quispe-Bravo, S., & Skamira, C. (2005). ADMA and oxidative stress may relate to the progression of renal disease: rationale and design of the VIVALDI study. Vascular Medicine (London, England), 10 Suppl 1, S97-102.
Böger RH, et al. ADMA and Oxidative Stress May Relate to the Progression of Renal Disease: Rationale and Design of the VIVALDI Study. Vasc Med. 2005;10 Suppl 1:S97-102. PubMed PMID: 16444875.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - ADMA and oxidative stress may relate to the progression of renal disease: rationale and design of the VIVALDI study. AU - Böger,Rainer H, AU - Schwedhelm,Edzard, AU - Maas,Renke, AU - Quispe-Bravo,Sabine, AU - Skamira,Cord, PY - 2006/2/1/pubmed PY - 2006/8/24/medline PY - 2006/2/1/entrez SP - S97 EP - 102 JF - Vascular medicine (London, England) JO - Vasc Med VL - 10 Suppl 1 N2 - The renin angiotensin system has been shown to be involved in the pathogenesis of vascular and renal sequelae of diabetes mellitus. In type 2 diabetes mellitus, angiotensin receptor blockers have been shown to exert clinical benefit by reducing the progression of diabetic nephropathy. They also improve endothelium-mediated vascular function. The latter effect is partly due to the reduction of angiotensin II-associated oxidative stress. Moreover, small clinical studies have shown that treatment with angiotensin receptor blockers also reduces the circulating levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthase. In the VIVALDI trial, the ability of the angiotensin receptor blocker telmisartan to reduce the progression of diabetic nephropathy (associated with proteinuria) in comparison with valsartan in more than 800 patients with type 2 diabetes during 1 year of treatment is being studied. In order to gain more detailed insight into the potential pathomechanisms associated with this effect, further end-points have been defined. Among these are the circulating levels of ADMA and the urinary excretion rate of 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha). The former is an endogenous inhibitor of NO-mediated vascular function(s) and a prospectively determined marker of major cardiovascular events and mortality; the latter is a lipid peroxidation product resulting from the nonenzymatic peroxidation of arachidonic acid, which exerts detrimental vascular effects similar to those of thromboxane A2. Urinary 8-iso-PGF2alpha has been shown in clinical studies to be an independent marker of cardiovascular disease. Highlighting the effects of telmisartan on ADMA and 8-iso-PGF levels in such a large cohort of diabetic patients will enhance our understanding of the roles of dysfunctional NO metabolism and redox mechanisms in the pathogenesis of end-organ damage and its prevention by pharmacotherapy with angiotensin receptor blockers. SN - 1358-863X UR - https://www.unboundmedicine.com/medline/citation/16444875/ADMA_and_oxidative_stress_may_relate_to_the_progression_of_renal_disease:_rationale_and_design_of_the_VIVALDI_study_ L2 - https://journals.sagepub.com/doi/10.1191/1358863x05vm608oa?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -