title: Sympathetic activation and contribution of genetic factors in hypertension with neurovascular compression of the rostral ventrolateral medulla.
abstract: OBJECTIVE
  The rostral ventrolateral medulla is an important center for the regulation of sympathetic and cardiovascular activities. Reportedly, neurovascular compression of the rostral ventrolateral medulla may be causally related to essential hypertension. We aimed to determine the mechanism behind elevated blood pressure in hypertensive patients with compression of the rostral ventrolateral medulla and to investigate whether genetic factors contribute to the etiology of hypertension with compression.
  
  
  METHODS
  The study included 56 patients with essential hypertension and 25 normotensive individuals. With the use of magnetic resonance imaging, the essential hypertension group was subdivided into hypertension with compression and without compression groups. We compared plasma levels of hormones that raise blood pressure and family histories of hypertension between the two hypertension groups and the normotension group.
  
  
  RESULTS
  Plasma norepinephrine levels, but not plasma renin activity, aldosterone, epinephrine, or vasopressin levels, were significantly higher in the hypertension with compression group (389+/-53 pg/ml) than in the hypertension without compression group (217+/-38, P<0.05) or in the normotension group (225+/-30, P<0.05). The percentage of individuals who had two hypertensive parents was significantly higher in the hypertension with compression group (39.4%) than in the hypertension without compression group (13.0%, P<0.05) or in the normotension group (8.0%, P<0.01).
  
  
  CONCLUSIONS
  These results indicate that neurovascular compression of the rostral ventrolateral medulla might be, at least in part, causally related to essential hypertension by increasing sympathetic nerve activity. They also suggest that genetic factors might contribute to the etiology of hypertension with neurovascular compression.
authors.affiliation: Second Department of Medicine, Research Institute for Neurological Diseases and Geriatrics, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Japan. morimot@koto.kpu-m.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Morimoto
authors.forename: S
authors.initials: S
authors.lastname: Sasaki
authors.forename: H
authors.initials: H
authors.lastname: Itoh
authors.forename: T
authors.initials: T
authors.lastname: Nakata
authors.forename: K
authors.initials: K
authors.lastname: Takeda
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
authors.forename: S
authors.initials: S
authors.lastname: Furuya
authors.forename: S
authors.initials: S
authors.lastname: Naruse
authors.forename: R
authors.initials: R
authors.lastname: Fukuyama
authors.forename: S
authors.initials: S
authors.lastname: Fushiki
mesh_terms: D000483:Alleles; D003251:Constriction, Pathologic; D005260:Female; D006728:Hormones / Q000097:blood; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000209:etiology / Q000235:genetics* / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D008499:Medical Records; D008526:Medulla Oblongata / Q000098:blood supply* / Q000473:pathology; D008875:Middle Aged; D009408:Nerve Compression Syndromes / Q000150:complications* / Q000175:diagnosis; D009638:Norepinephrine / Q000097:blood; D012016:Reference Values; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014652:Vascular Diseases / Q000150:complications* / Q000175:diagnosis
chemical_list: D006728:Hormones; D009638:Norepinephrine