title: Relationship of neurovascular compression to central sympathetic discharge and essential hypertension.
abstract: OBJECTIVE
  We planned to examine the relationship between neurovascular compression (NVC) of the rostral ventrolateral medulla (RVLM) and the magnitude of central sympathetic hyperactivity in normal subjects and in patients with untreated and uncomplicated essential hypertension (EHT).
  
  
  BACKGROUND
  Previously it has not been possible to establish a definitive relationship between EHT and NVC of the RVLM, a location containing efferent sympathetic vasoconstrictor neurons. Furthermore, the relationship between NVC and magnitude of sympathetic nerve hyperactivity has not been adequately examined, despite the knowledge that hyperactivity varies according to EHT severity.
  
  
  METHODS
  In 83 subjects, we used magnetic resonance imaging to detect NVC and, independently, peroneal microneurography to quantify muscle sympathetic nerve activity (MSNA), expressed as the mean frequency of multi-unit discharge (m-MSNA) and of single units (s-MSNA). Subjects were classified according to arterial pressure values into groups with normal (NT) (n = 24) or high-normal (HN) (n = 14) arterial pressure and mild (EHT-1) (n = 26) or severe (EHT-2/3) (n = 19) EHT.
  
  
  RESULTS
  A significantly greater sympathetic activity was found in 23 subjects with NVC, compared with 60 subjects without NVC. The prevalence of NVC and the magnitude of sympathetic hyperactivity were greater in the EHT-1 group (p < 0.05) than in the other three groups. There was no significant difference in confounding variables between the groups. Although increased sympathetic activity was strongly predictive of NVC, this was not significantly related to baroreceptor sensitivity controlling the pulse interval (cardiac baroreceptor reflex sensitivity).
  
  
  CONCLUSIONS
  Neurovascular compression of the RVLM may cause central sympathetic activation in normal and hypertensive populations and therefore has significant implications regarding the pathogenesis of EHT.
authors.affiliation: Department of Cardiology, Leeds Teaching Hospitals, Leeds, United Kingdom. paul.smith@ukgateway.net
authors.forename: Paul A
authors.initials: PA
authors.lastname: Smith
authors.forename: James F M
authors.initials: JF
authors.lastname: Meaney
authors.forename: Lee N
authors.initials: LN
authors.lastname: Graham
authors.forename: John B
authors.initials: JB
authors.lastname: Stoker
authors.forename: Alan F
authors.initials: AF
authors.lastname: Mackintosh
authors.forename: David A S G
authors.initials: DA
authors.lastname: Mary
authors.forename: Stephen G
authors.initials: SG
authors.lastname: Ball
mesh_terms: D000328:Adult; D000368:Aged; D002561:Cerebrovascular Disorders / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008526:Medulla Oblongata / Q000503:physiopathology*; D008875:Middle Aged; D009408:Nerve Compression Syndromes / Q000150:complications / Q000503:physiopathology*; D011446:Prospective Studies; D013564:Sympathetic Nervous System / Q000503:physiopathology*