Open AccessCause and Consequences of Sympathetic Hyperactivity in Chronic Kidney Disease
Author(s) -
Peter Kotanko
Publication year - 2005
Publication title -
blood purification
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 57
eISSN - 1421-9735
pISSN - 0253-5068
DOI - 10.1159/000089444
Subject(s) - medicine , moxonidine , sympathetic nervous system , kidney disease , hemodialysis , asymmetric dimethylarginine , endocrinology , clonidine , rilmenidine , population , blood pressure , receptor , agonist , chemistry , biochemistry , environmental health , amino acid , arginine
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 beta-blockers and centrally acting sympatholytic drugs on cardiovascular mortality in chronic kidney disease and hemodialysis patients are very much needed.