title: Amelioration of vascular endothelial dysfunction in obstructive sleep apnea syndrome by nasal continuous positive airway pressure--possible involvement of nitric oxide and asymmetric NG, NG-dimethylarginine.
abstract: BACKGROUND
  Asymmetric NG,NG-dimethylarginine (ADMA) is an endogenous inhibitor of endothelial nitric oxide (NO) synthase and its plasma concentration is elevated in patients with cardiovascular risk factors, including hyperlipidemia, hypertension, diabetes, and hyperhomocysteinemia. Obstructive sleep apnea syndrome (OSAS) has been attracting attention as a risk factor for cardiovascular disorders because it often accompanies hypertension, obesity, glucose impairment, and dyslipidemia, all of which are factors in metabolic syndrome and risk factors for cardiovascular disease.
  
  
  RESULTS
  In the present study, flow-mediated vasodilatation (FMD) of the brachial artery and plasma concentrations of ADMA were measured before and after nasal continuous positive airway pressure (nCPAP) therapy, which abrogates apnea, in 10 male patients aged 36-69 years old, who were given a diagnosis of OSAS by polysomnography. The percent FMD (%FMD) improved significantly from 3.3+/-0.3% to 5.8+/-0.4% (p<0.01) and 6.6+/-0.3% (p<0.01), before, 1 week, and 4 weeks after nCPAP, respectively. At the same time, the plasma NOx concentrations, metabolites of NO, tended to increase, but the plasma ADMA concentration decreased inversely to %FMD and NOx. A negative correlation between %FMD and plasma ADMA concentration, and a positive correlation between %FMD and plasma NOx concentrations were observed.
  
  
  CONCLUSIONS
  Nasal CPAP improves endothelial function, in part by the decreasing ADMA concentration, thereby potentiating NO production.
authors.affiliation: Department of Geriatric Medicine, University of Tokyo Graduate School of Medicine, Japan.
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Ohike
authors.forename: Koichi
authors.initials: K
authors.lastname: Kozaki
authors.forename: Katsuya
authors.initials: K
authors.lastname: Iijima
authors.forename: Masato
authors.initials: M
authors.lastname: Eto
authors.forename: Taro
authors.initials: T
authors.lastname: Kojima
authors.forename: Eijiro
authors.initials: E
authors.lastname: Ohga
authors.forename: Tomofumi
authors.initials: T
authors.lastname: Santa
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Imai
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Hashimoto
authors.forename: Masao
authors.initials: M
authors.lastname: Yoshizumi
authors.forename: Yasuyoshi
authors.initials: Y
authors.lastname: Ouchi
mesh_terms: D000328:Adult; D000368:Aged; D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood; D001916:Brachial Artery / Q000502:physiology; D045422:Continuous Positive Airway Pressure; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009566:Nitrates / Q000032:analysis; D009569:Nitric Oxide / Q000096:biosynthesis; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052250:Nitric Oxide Synthase Type III; D009573:Nitrites / Q000032:analysis; D020181:Sleep Apnea, Obstructive / Q000628:therapy*; D014664:Vasodilation
chemical_list: D009566:Nitrates; D009573:Nitrites; C487735:dimethylarginine; D009569:Nitric Oxide; D001120:Arginine; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III