title: Sympathetic control of the circulation in hypertension: lessons from autonomic disorders.
abstract: OBJECTIVE
  Inappropriate sympathetic overactivity is consistently observed in patients with essential hypertension. The present review summarizes the recent advances that have been made in our understanding of the role of the sympathetic nervous system in hypertension.
  
  
  RESULTS
  Studies in patients with autonomic disorders underscore the role of the sympathetic nervous system in the long-term maintenance of hypertension. Abnormalities in the afferent limb of the sympathetic nervous system, in the regulation of central neurons where sympathetic outflow originates, and in the modulation of efferent sympathetic function, can all produce autonomic disorders that are associated with hypertension. More subtle dysfunctions in any of these components have been described in essential hypertension and can contribute to its pathogenesis. These include impaired buffering capacity of arterial baroreflexes, increased central sympathetic outflow, and enhanced norepinephrine release (or decrease reuptake) from sympathetic nerve terminals. Whether genetic polymorphisms of adrenoreceptors are associated with essential hypertension is an area of active research.
  
  
  CONCLUSIONS
  Increased sympathetic activity can contribute to sustained hypertension not only because of its hemodynamic effects (increased cardiac output and vascular resistance), but also by altering renal and water handling by the kidney, and by inducing cardiac and vascular remodeling. Antihypertensive agents that directly or indirectly target this sympathetic overactivity may be particularly useful in long-term treatment of essential hypertension.
authors.affiliation: Department of Medicine and Pharmacology, Division of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee 37212, USA. Italo.biaggioni@vanderbilt.edu
authors.forename: Italo
authors.initials: I
authors.lastname: Biaggioni
mesh_terms: D000818:Animals; D017704:Baroreflex / Q000502:physiology; D004195:Disease Models, Animal; D004525:Efferent Pathways / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology*; D008297:Male; D011110:Polymorphism, Genetic; D011311:Pressoreceptors / Q000502:physiology; D011379:Prognosis; D051381:Rats; D011918:Rats, Inbred SHR; D011941:Receptors, Adrenergic / Q000235:genetics*; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D013564:Sympathetic Nervous System / Q000502:physiology*; D014655:Vascular Resistance
chemical_list: D011941:Receptors, Adrenergic