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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:2685-2686
doi: 10.1161/01.ATV.0000193890.94720.1a
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:2685.)
© 2005 American Heart Association, Inc.


Letters to the Editor

Letter to the Editor

Dissociation Between the Short-Term Effects of Nocturnal Hemodialysis on Endothelium Dependent Vasodilation and Plasma ADMA

Christopher T. Chan; Paula J. Harvey

Department of Medicine, University Health Network and Mount Sinai Hospital University of Toronto, Ontario, Canada

Rainer Böger

Clinical Pharmacology Unit, Institute of Experimental and Clinical Pharmacology Center of Experimental Medicine University Hospital Hamburg–Eppendorf, Germany

Andreas Pierratos

Humber River Regional Hospital University of Toronto, Ontario, Canada

John S. Floras

Department of Medicine, University Health Network and Mount Sinai Hospital University of Toronto, Ontario, Canada


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor,

Cardiovascular mortality remains the leading cause of death in ESRD patients.1 Several of the abnormalities that accrue in ESRD have the potential to attenuate endothelium-dependent vasodilation (EDV).2 These include, but are not restricted to, uremia, hypertension, and increased plasma concentrations of asymmetrical dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthase3,4 that has been recently associated independently with increased cardiovascular event rates.5

Nocturnal hemodialysis (NHD) (5 to 6 sessions per week, 8 hours per session) is a novel mode of renal replacement therapy that increases both the frequency and dose of dialysis.6 Within 1 to 2 months after ESRD patients are converted from CHD to NHD, hypertension resolves, EDV improves markedly, and vasodilator responsiveness to sublingual glyceryl trinitrate (GTN) is enhanced.7

ADMA inhibits competitively all 3 isoforms of NO synthase.8 When infused into healthy humans, ADMA decreases forearm blood flow and cardiac output and increases systemic vascular resistance.9,10 ADMA accumulates with renal failure.11 Its plasma concentrations are elevated in patients receiving CHD.12 We therefore tested the hypotheses that NHD improves EDV by lowering plasma concentrations of ADMA.

Seventeen nonsmoking ESRD patients (10 men; mean age, 41±2 years) were studied, after informed written consent, according to methods detailed in the online supplement (available at http://atvb.ahajournals.org). While on CHD, these patients required, on average, 2.6 antihypertensive drugs for blood pressure control. Hyperemia did not elicit a consistent increase in flow-mediated dilation of the brachial artery (–2.9±2.0% change in diameter). Furthermore, the vasodilator response to GTN was less than . . . [Full Text of this Article]