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(Hypertension. 2008;51:755.)
© 2008 American Heart Association, Inc.

Original Articles

Salt Loading Increases Urinary Excretion of Linoleic Acid Diols and Triols in Healthy Human Subjects

Albert W. Dreisbach; Janet C. Rice; Shanker Japa; John W. Newman; Aster Sigel; Rajan S. Gill; Arthur E. Hess; Angela C. Cemo; Juan P. Fonseca; Bruce D. Hammock; Juan J.L. Lertora; L. Lee Hamm

From the Department of Medicine (A.W.D., S.J., A.S., A.E.H., J.P.F., J.J.L.L., L.L.H.), Tulane Health Science Center, New Orleans, La; Department of Biostatistics (J.C.R.), Tulane School of Public Health, New Orleans, La; Tulane-Louisiana State University-Charity Hospital General Clinical Research Center (S.J., A.C.C., J.J.L.L.), New Orleans; Departments of Entomology (J.W.N., R.S.G., B.D.H.) and Nutrition (J.W.N., R.S.G.), University of California, Davis; Western Human Nutrition Research Center (J.W.N.), US Department of Agriculture, Davis, Calif. Current addresses: National Institutes of Health Clinical Center (J.J.L.L.), Bethesda, Md; Division of Nephrology (A.W.D.), Department of Medicine, University of Mississippi Medical Center, Jackson.

Correspondence to Albert W. Dreisbach, Division of Nephrology, Department of Medicine, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216. E-mail adreisbach{at}umsmed.edu

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 F1 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.

Key Words: linoleic acid • hypertension • salt loading • salt excretion • prostacyclin • PGE2