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"One of the earliest signs of vascular change is endothelial dysfunction, which is also known to provoke albuminuria and to predict cardiovascular prognosis," write Roland E. Schmieder, MD, FACC, from the University of Erlangen-Nürnberg in Germany, and colleagues. "The aim of this study was to analyze the effects of renin-angiotensin system (RAS) blockade on renal endothelial function."
In this multicenter, prospective, double-blind, forced-titration study, 96 patients with type 2 diabetes, hypertension, glomerular filtration rate greater than 80 mL/minute, and normoalbuminuria or microalbuminuria were randomized to once daily treatment with 40/80 mg of telmisartan or 5/10 mg of ramipril for 9 weeks. Nitric oxide activity was estimated using the decline in renal plasma flow (RPF) in response to intravenous NG-monomethyl-L-arginine (L-NMMA).
The mean fall in RPF in response to L-NMMA increased with telmisartan from 71.9 ± 9.0 mL/minute before therapy to 105.2 ± 9.7 mL/minute at the end of treatment (P < .001). With ramipril, RPF response to L-NMMA increased from 60.1 ± 12.2 to 87.8 ± 9.2 mL/minute (P = .018; adjusted difference between treatments, -17.1 ± 13.7 mL/minute; P = .214).
Without L-NMMA, telmisartan increased RPF at rest from 652.0 ± 27.0 to 696.1 ± 31.0 mL/minute (P = .047). In contrast, ramipril produced no significant changes in RPF. The greater the improvement in basal NO activity, the greater was the vasodilatory effect on renal vasculature (r = 0.47; P < .001).
"In patients with type 2 diabetes, telmisartan and ramipril both increased NO activity of the renal endothelium significantly, which in turn may support the preservation of cardiovascular and renal function," the authors write.
Boehringer Ingelheim, Bayer AG, and GlaxoSmithKline sponsored this study. The costs of publication of the current study were defrayed in part by the payment of page charges, mandating its being marked "advertisement" solely to indicate this fact.
Diabetes Care. 2007;30:1351-1356.
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