title: Salt loading increases urinary excretion of linoleic acid diols and triols in healthy human subjects.
abstract: Increased dietary linoleic acid has been associated with reduced blood pressure in clinical and animal studies possibly mediated by prostaglandins. Urinary linoleate and prostaglandin metabolite excretion were investigated in subjects exposed to a salt-loading/salt-depletion regimen. Twelve healthy subjects were recruited from the New Orleans population (before Hurricaine Katrina) and admitted to the Tulane-Louisiana State University-Charity Hospital General Clinical Research Center after a 5-day outpatient lead-in phase on a 160-mmol sodium diet. On inpatient day 1, the subjects were maintained on the 160-mmol sodium diet, and a 24-hour urine specimen was collected. On day 2, the subjects received 2 L of IV normal saline over 4 hours and continued on a 160-mmol Na(+) diet (total: 460 mmol of sodium). Two 12-hour urine collections were obtained. On day 3, the subjects received three 40-mg oral doses of furosemide, two 12-hour urine collections were obtained, and the subjects were given a 10-mmol sodium diet. Urinary oxidized lipids were measured by high-performance liquid chromatography-tandem quadrupole mass spectroscopy. The excretion of the urinary linoleate metabolites, dihydroxyoctadecamonoenoic acids, and trihydroxyoctadecamonoenoic acids increased significantly during intravenous salt loading as compared with day 1 and the salt-depleted periods. The urinary excretion of 6-keto- prostaglandin F1alpha was unaffected by salt loading but was dramatically increased 7- to 10-fold by salt depletion. Prostaglandin E2 excretion was positively correlated with sodium excretion. The salt-stimulated production of linoleic acid diols and triols may inhibit tubular sodium reabsorption, thereby assisting in the excretion of the sodium load.
authors.affiliation: Department of Medicine, Tulane Health Science Center, New Orleans, La., USA. adreisbach@umsmed.edu
authors.forename: Albert W
authors.initials: AW
authors.lastname: Dreisbach
authors.forename: Janet C
authors.initials: JC
authors.lastname: Rice
authors.forename: Shanker
authors.initials: S
authors.lastname: Japa
authors.forename: John W
authors.initials: JW
authors.lastname: Newman
authors.forename: Aster
authors.initials: A
authors.lastname: Sigel
authors.forename: Rajan S
authors.initials: RS
authors.lastname: Gill
authors.forename: Arthur E
authors.initials: AE
authors.lastname: Hess
authors.forename: Angela C
authors.initials: AC
authors.lastname: Cemo
authors.forename: Juan P
authors.initials: JP
authors.lastname: Fonseca
authors.forename: Bruce D
authors.initials: BD
authors.lastname: Hammock
authors.forename: Juan J L
authors.initials: JJ
authors.lastname: Lertora
authors.forename: L Lee
authors.initials: LL
authors.lastname: Hamm
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000652:urine; D000328:Adult; D015232:Dinoprostone / Q000652:urine; D005260:Female; D005665:Furosemide / Q000494:pharmacology; D006801:Humans; D019787:Linoleic Acid / Q000378:metabolism / Q000652:urine*; D008297:Male; D008875:Middle Aged; D012964:Sodium / Q000652:urine; D049994:Sodium Potassium Chloride Symporter Inhibitors / Q000494:pharmacology; D012982:Sodium, Dietary / Q000494:pharmacology*; D013997:Time Factors
chemical_list: D049994:Sodium Potassium Chloride Symporter Inhibitors; D012982:Sodium, Dietary; D015121:6-Ketoprostaglandin F1 alpha; D005665:Furosemide; D019787:Linoleic Acid; D012964:Sodium; D015232:Dinoprostone