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J Am Coll Cardiol, 2005; 46:518-523, doi:10.1016/j.jacc.2005.04.040 (Published online 14 July 2005).
© 2005 by the American College of Cardiology Foundation
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Asymmetric Dimethylarginine, L-Arginine, and Endothelial Dysfunction in Essential Hypertension

Francesco Perticone, MD*,*, Angela Sciacqua, MD*, Raffaele Maio, MD*, Maria Perticone, MD*, Renke Maas, MD{dagger}, Rainer H. Boger, MD{dagger}, Giuseppe Tripepi, Stat Tech{ddagger}, Giorgio Sesti, MD* and Carmine Zoccali, MD{ddagger}

* Internal Medicine and Cardiovascular Diseases Unit, Department of Medicina Sperimentale e Clinica "G. Salvatore," University Magna Graecia of Catanzaro, Catanzaro, Italy
{dagger} Clinical Pharmacology Unit, Department of Pharmacology, University Hospital Hamburg-Eppendorf, Hamburg-Eppendorf, Germany
{ddagger} CNR-IBIM, National Research Council-Institute of Biomedicine, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension, Reggio Calabria, Italy



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Figure 1 Relationship between L-arginine (L-Arg) and asymmetric dimethylarginine (ADMA) in both normotensive subjects (NTs) (open circles) and hypertensive patients (HTs) (solid circles). In the whole population (r = 0.626; p < 0.0001) and in the HT group (r = 0.545; p < 0.001), the two covariates resulted linearly correlated; no relationship was found in the NT group.

 


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Figure 2 Forearm blood flow (FBF) increase during infusion of acetylcholine (ACh). As shown, ACh-stimulated FBF was significantly reduced in hypertensive subjects (HTs) in comparison to normotensive control (NTs) subjects. Intra-arterial coinfusion of L-arginine (L-Arg) induced a further significant enhancement in ACh-stimulated vasodilation in HT patients.

 


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Figure 3 In this figure the correlation between asymmetric dimethylarginine (ADMA) levels and the peak increase in acetylcholine-stimulated forearm blood flow is reported in hypertensive patients.

 




 
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