title: The role of melatonin in the pathogenesis of hypertension in rats with metabolic syndrome.
abstract: BACKGROUND
  Melatonin, the primary hormone of the pineal gland, is a known modulator of various physiological processes. The aim of this study was to evaluate the role of melatonin in the pathogenesis of hypertension in rats with metabolic syndrome and to assess whether melatonin supplementation prevents the development of hypertension in this model.
  
  
  METHODS
  Twenty male Sprague-Dawley (SD) rats were fed either a high fructose diet (n = 10) or a regular diet (control; n = 10) for 5 weeks. Urinary excretion of 6-hydroxymelatoninsulfate (a metabolite of melatonin) was measured at the beginning and the end of the study. An additional 20 SD rats were fed with the same diets but with a supplementation of melatonin (30 mg/kg/day) in their drinking water. Blood pressure (BP) was measured every week.
  
  
  RESULTS
  BP increased significantly in rats fed with a high fructose diet and remained unchanged in the control group. The BP rise was associated with a significant decrease in melatonin secretion during sleep. Melatonin supplementation prevented the BP rise in fructose fed rats. BP increased by 14.6 +/- 1.0 mm Hg in the fructose fed rats, whereas it increased by only 3 +/- 2.6 mm Hg in rats fed with fructose and melatonin (P < 0.001 between groups).
  
  
  CONCLUSIONS
  Melatonin secretion decreased in fructose fed rats that developed hypertension. Administration of melatonin blunted this BP rise. These data suggested that melatonin plays a role in the pathogenesis of hypertension in rats with metabolic syndrome.
authors.affiliation: Department of Internal Medicine D and the Hypertension unit, The Chaim Sheba medical center, Tel-Hashomer, affiliated to Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
authors.forename: Avshalom
authors.initials: A
authors.lastname: Leibowitz
authors.forename: Edna
authors.initials: E
authors.lastname: Peleg
authors.forename: Yhenoatan
authors.initials: Y
authors.lastname: Sharabi
authors.forename: Zehava
authors.initials: Z
authors.lastname: Shabtai
authors.forename: Ari
authors.initials: A
authors.lastname: Shamiss
authors.forename: Ehud
authors.initials: E
authors.lastname: Grossman
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D019422:Dietary Sucrose / Q000494:pharmacology; D019587:Dietary Supplements; D004195:Disease Models, Animal; D005632:Fructose / Q000008:administration & dosage / Q000494:pharmacology; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology* / Q000517:prevention & control; D008297:Male; D008550:Melatonin / Q000494:pharmacology / Q000502:physiology* / Q000652:urine; D024821:Metabolic Syndrome / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000097:blood
chemical_list: D019422:Dietary Sucrose; D014280:Triglycerides; D005632:Fructose; D008550:Melatonin