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Published ahead of print on February 16, 2005
J Am Soc Nephrol 16: 1135-1140, 2005
© 2005 American Society of Nephrology
doi: 10.1681/ASN.2004100852
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Chronic Kidney Disease

Chronic Angiotensin II Receptor Blockade Reduces (Intra)Renal Vascular Resistance in Patients with Type 2 Diabetes

Danilo Fliser*, Kathrin-Kristin Wagner*, Astrid Loos*, Dimitrios Tsikas{dagger} and Hermann Haller*

* Department of Internal Medicine and {dagger} Institute of Clinical Pharmacology, Medical School Hannover, Hannover, Germany

Address correspondence to: Dr. Danilo Fliser, Department of Internal Medicine, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany. Phone: 49-511-532-6319; Fax: 49-511-55-2366; E-mail:fliser.danilo{at}mh-hannover.de

Received for publication October 15, 2004. Accepted for publication December 29, 2004.

Increased (intra)renal activity of the renin-angiotensin system may cause a persistent increase in renovascular resistance and intraglomerular pressure in patients with diabetes, thus contributing to the development of diabetic renal damage. The effect of chronic angiotensin II subtype 1 receptor blockade on (intra)renal hemodynamics in patients with type 2 diabetes was examined in a double-blind parallel group study. Patients were treated with 40 mg of olmesartan (n = 19) or placebo (n = 16), and renal hemodynamics were assessed before and after 12 wk of treatment using inulin and para-aminohippurate clearance techniques. Olmesartan significantly reduced 24-h ambulatory systolic and diastolic BP (both P < 0.05). In parallel, effective renal plasma flow increased significantly from 602 ± 76 to 628 ± 87 ml/min per 1.73 m2, whereas filtration fraction and renovascular resistance decreased significantly (all P < 0.05). With placebo treatment, effective renal plasma flow decreased and filtration fraction increased significantly (both P < 0.05). GFR was not affected by both treatments. Active plasma renin concentration increased considerably (P < 0.05) with olmesartan therapy but remained unchanged with placebo treatment. Nitric oxide metabolism (plasma nitrate and nitrite) and asymmetric dimethylarginine blood levels were not affected by olmesartan and placebo therapy. In contrast, plasma 8-isoprostane 15(S)-8-iso-prostaglandin F2a concentration, a biochemical marker of oxidative stress, decreased significantly (P < 0.05) with olmesartan treatment. Chronic angiotensin II subtype 1 receptor blockade decreases (intra)renal vascular resistance and increases renal perfusion despite significant BP reduction. In addition, it significantly reduces oxidative stress. These effects of angiotensin II receptor antagonists may contribute to their beneficial long-term renal effects in patients with type 2 diabetes.




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