title: Circulating coupling factor 6 in human hypertension: role of reactive oxygen species.
abstract: OBJECTIVE
  Coupling factor 6 is an endogenous inhibitor of prostacyclin synthesis and might function as an endogenous vasoconstrictor in the fashion of a circulating hormone in rats. We investigated the role of coupling factor 6 in human hypertension.
  
  
  RESULTS
  The patients with essential hypertension (EH) (n = 30) received a series of normal salt diet (12 g salt/day) for 3 days, low salt diet (2 g salt/day) for 7 days, and high salt diet (20-23 g salt/day) for 7 days. Normotensive control subjects (n = 27) received normal and low salt diets. The plasma level of coupling factor 6, measured by radioimmunoassay, during normal salt diet was higher in patients with EH than in normotensive subjects (17.6 +/- 1.7 versus 12.8 +/- 0.5 ng/ml, P < 0.01). Whereas the plasma level of coupling factor 6 was unchanged after salt restriction in normotensive subjects, it was decreased after salt restriction (from 12 g/day to 2 g/day) and was increased after salt loading (from 2 g/day to 20-23 g/day) in patients with EH. This increase in plasma level of coupling factor 6 was abolished by oral administration of ascorbic acid, but the level of blood pressure was unaffected. The percentage changes in plasma coupling factor 6 level after salt restriction and loading were positively correlated with those in mean blood pressure (r = 0.57, P < 0.01), and negatively correlated with those in plasma nitric oxide level (r = -0.51, P < 0.05).
  
  
  CONCLUSIONS
  These indicate that circulating coupling factor 6 is elevated in human hypertension and modulated by salt intake presumably via reactive oxygen species.
authors.affiliation: Second Deparment of Internal Medicine, Hirosaki University School of Medicine, Japan. osanait@cc.hirosaki-u.ac.jp
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Osanai
authors.forename: Satoko
authors.initials: S
authors.lastname: Sasaki
authors.forename: Takaatsu
authors.initials: T
authors.lastname: Kamada
authors.forename: Naoto
authors.initials: N
authors.lastname: Fujiwara
authors.forename: Takao
authors.initials: T
authors.lastname: Nakano
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Tomita
authors.forename: Toshiro
authors.initials: T
authors.lastname: Matsunaga
authors.forename: Koji
authors.initials: K
authors.lastname: Magota
authors.forename: Ken
authors.initials: K
authors.lastname: Okumura
mesh_terms: D000975:Antioxidants / Q000008:administration & dosage; D001205:Ascorbic Acid / Q000008:administration & dosage; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D004039:Diet, Sodium-Restricted; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D025261:Mitochondrial Proton-Translocating ATPases / Q000097:blood* / Q000187:drug effects; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D010086:Oxidative Phosphorylation Coupling Factors / Q000097:blood* / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D012083:Renin / Q000378:metabolism; D012982:Sodium, Dietary / Q000008:administration & dosage; D013223:Statistics as Topic
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D009566:Nitrates; D009573:Nitrites; D010086:Oxidative Phosphorylation Coupling Factors; D017382:Reactive Oxygen Species; D012982:Sodium, Dietary; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; D012083:Renin; C000628217:F(6) ATPase; D025261:Mitochondrial Proton-Translocating ATPases; D001205:Ascorbic Acid; D009638:Norepinephrine