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Cause and Consequences of Sympathetic Hyperactivity in Chronic Kidney Disease

Kotanko P.

Author affiliations

Renal Research Institute, New York, N.Y., USA

Corresponding Author

Peter Kotanko, MD

Renal Research Institute

207 East 94th Street, Suite 303

New York, NY 10128 (USA)

Tel. +1 646 672 4042, Fax +1 646 672 4174, E-Mail pkotanko@rriny.com

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Abstract

Patients with chronic kidney disease and patients undergoing hemodialysis treatment show a sustained overactivity of the sympathetic nervous system, which originates from signals arising in the failing kidneys and traveling via afferent renal nerves to cardiovascular centers in the brainstem. Additional important factors are increased levels of angiotensin II and asymmetrical dimethylarginine. The sympathetic overactivity contributes to hypertension and cardiovascular morbidity and mortality in that patient population. Sympathetic overactivity can be reduced by adrenergic receptor blockers, centrally acting sympathicolytic drugs such as moxonidine and rilmenidine, angiotensin-converting enzyme inhibition, and angiotensin II type 1 receptor antagonists. Daily short hemodialysis and long nocturnal hemodialysis may reduce the elevated sympathetic activity, possibly because of an increased clearance of asymmetrical dimethylarginine, an endogenous nitric oxide synthase inhibitor. Prospective trials examining the potential impact of both β-blockers and centrally acting sympatholytic drugs on cardiovascular mortality in chronic kid ney disease and hemodialysis patients are very much needed.

© 2006 S. Karger AG, Basel


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Article / Publication Details

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Abstract of Paper

Published online: December 23, 2005
Issue release date: December 2005

Number of Print Pages: 5
Number of Figures: 1
Number of Tables: 0

ISSN: 0253-5068 (Print)
eISSN: 1421-9735 (Online)

For additional information: https://www.karger.com/BPU


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