title: D-allose, an all-cis aldo-hexose, suppresses development of salt-induced hypertension in Dahl rats.
abstract: OBJECTIVE
  D-allose, an all-cis aldo-hexose, is non-caloric and possesses antioxidant properties. We investigated the effects of oral D-allose supplementation on the development of high blood pressure and the oxidative status in two genetically hypertensive animal models: Dahl salt-sensitive hypertensive (DS) rats and spontaneously hypertensive rats.
  
  
  RESULTS
  The systolic blood pressure of DS rats fed a 4% salt diet for 4 weeks significantly increased from 122+/-8 to 161+/-5 mmHg as compared with DS rats fed a normal salt diet (138+/-5 mmHg at 4 weeks), whereas concordant supplementation of D-allose, but not D-glucose, with a dose of 2 g/kg daily to salt-loaded DS rats suppressed the development of high blood pressure (135+/-7 mmHg at 4 weeks), accompanied with decreases in superoxide production in the aorta that was determined by the lucigenin chemiluminescence and dihydroethidium staining. The increases of urinary protein secretion of salt-loaded DS rats were prevented by D-allose supplementation (DS rats fed 0.5% salt, 18.2+/-6.3 mg/day; DS rats fed 4% salt alone, 81.8+/-16.5 mg/day; DS rats fed 4% salt+D-allose, 31.3+/-11.8 mg/day; DS rats fed 4% salt+D-glucose, 85.3+/-20.5 mg/day). On the other hand, D-allose supplementation in spontaneously hypertensive rats had no significant effect on the blood pressure or the aortic superoxide production during the early developing stage of hypertension.
  
  
  CONCLUSIONS
  These results underscore the role of enhanced oxidative stress in the pathogenesis of high blood pressure development in DS rats, and suggest the possibility of D-allose supplementation for prevention of salt-sensitive hypertension.
authors.affiliation: Department of Pharmacology, Kagawa University Medical School, Kagawa, Japan. kimura@kms.ac.jp
authors.forename: Shoji
authors.initials: S
authors.lastname: Kimura
authors.forename: Guo-Xing
authors.initials: GX
authors.lastname: Zhang
authors.forename: Akira
authors.initials: A
authors.lastname: Nishiyama
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Nagai
authors.forename: Toshitaka
authors.initials: T
authors.lastname: Nakagawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Miyanaka
authors.forename: Yoshihide
authors.initials: Y
authors.lastname: Fujisawa
authors.forename: Akira
authors.initials: A
authors.lastname: Miyatake
authors.forename: Tsubasa
authors.initials: T
authors.lastname: Nagai
authors.forename: Masaaki
authors.initials: M
authors.lastname: Tokuda
authors.forename: Youichi
authors.initials: Y
authors.lastname: Abe
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D019587:Dietary Supplements; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D005947:Glucose / Q000008:administration & dosage / Q000627:therapeutic use*; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D007668:Kidney / Q000473:pathology; D007672:Kidney Cortex / Q000378:metabolism; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D009206:Myocardium / Q000473:pathology; D019255:NADPH Oxidases / Q000235:genetics; D009929:Organ Size / Q000187:drug effects; D010766:Phosphorylation / Q000187:drug effects; D011507:Proteinuria / Q000517:prevention & control / Q000652:urine; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D020303:Rats, Inbred Dahl; D011918:Rats, Inbred SHR; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D013481:Superoxides / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D017673:Sodium Chloride, Dietary; D013481:Superoxides; C002055:allose; D019255:NADPH Oxidases; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D005947:Glucose