title: Sympathetic overactivity in hypertension and cardiovascular disease.
abstract: From the first description of its anatomy by T. Willis to the novel therapeutic manipulations, it is unanimously recognized that the sympathetic nervous system (SNS) holds a crucial role in cardiovascular homeostasis. The introduction of sophisticated techniques, as microneurography and regional norepinephrine spillover provided the evidence for the role of sympathetic overactivity in various cardiovascular disease entities. Sympathetic activation is common in patients with essential hypertension and contributes to initiation, maintenance and progression of the disease and it contributes to the manifestation of its major complications. A considerable body of evidence relates SNS overactivity with high sodium intake in experimental animals and humans and the underlying mechanisms have nowadays been elucidated. SNS activity is more pronounced in patients with resistant hypertension and there are several conditions that lead to this phenomenon, as older age, kidney disease, obesity and metabolic syndrome, mental stress and sleep apnea. SNS overactivity holds also a key physiopathological role in heart failure, acute coronary syndromes and arrhythmias. Moreover, inhibition of sympathetic overactivity by various means, including central SNS suppressing drugs, peripheral alpha- and beta- adrenergic receptor blockers, or novel approaches as renal sympathetic denervation have been used successfully in the treatment of all these disorders.
authors.forename: A J
authors.initials: AJ
authors.lastname: Manolis
authors.forename: L E
authors.initials: LE
authors.lastname: Poulimenos
authors.forename: M S
authors.initials: MS
authors.lastname: Kallistratos
authors.forename: I
authors.initials: I
authors.lastname: Gavras
authors.affiliation: Department of Cardiology, Asklepeion General Hospital, 1 Vas. Pavlou Ave, Voula 16673, Greece. ajmanol@otenet.gr.
authors.forename: H
authors.initials: H
authors.lastname: Gavras
mesh_terms: D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology*; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*