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

Research output: Contribution to journalArticle

8 Citations (Scopus)

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 F1α 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.

Original languageEnglish (US)
Pages (from-to)755-761
Number of pages7
JournalHypertension
Volume51
Issue number3
DOIs
StatePublished - Mar 2008

Fingerprint

Linoleic Acid
Healthy Volunteers
Salts
Sodium
Diet
Urine Specimen Collection
Prostaglandins
Charities
State Hospitals
Acids
Furosemide
Dinoprostone
Inpatients
Mass Spectrometry
Outpatients
High Pressure Liquid Chromatography
Urine
Blood Pressure
Lipids
Research

Keywords

  • Hypertension
  • Linoleic acid
  • PGE2
  • Prostacyclin
  • Salt excretion
  • Salt loading

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Dreisbach, A. W., Rice, J. C., Japa, S., Newman, J. W., Sigel, A., Gill, R. S., ... Hamm, L. L. (2008). Salt loading increases urinary excretion of linoleic acid diols and triols in healthy human subjects. Hypertension, 51(3), 755-761. https://doi.org/10.1161/HYPERTENSIONAHA.107.100123

Salt loading increases urinary excretion of linoleic acid diols and triols in healthy human subjects. / Dreisbach, Albert W.; Rice, Janet C.; Japa, Shanker; Newman, John W.; Sigel, Aster; Gill, Rajan S.; Hess, Arthur E.; Cemo, Angela C.; Fonseca, Juan P.; Hammock, Bruce D.; Lertora, Juan J L; Hamm, L. Lee.

In: Hypertension, Vol. 51, No. 3, 03.2008, p. 755-761.

Research output: Contribution to journalArticle

Dreisbach, AW, Rice, JC, Japa, S, Newman, JW, Sigel, A, Gill, RS, Hess, AE, Cemo, AC, Fonseca, JP, Hammock, BD, Lertora, JJL & Hamm, LL 2008, 'Salt loading increases urinary excretion of linoleic acid diols and triols in healthy human subjects', Hypertension, vol. 51, no. 3, pp. 755-761. https://doi.org/10.1161/HYPERTENSIONAHA.107.100123
Dreisbach, Albert W. ; Rice, Janet C. ; Japa, Shanker ; Newman, John W. ; Sigel, Aster ; Gill, Rajan S. ; Hess, Arthur E. ; Cemo, Angela C. ; Fonseca, Juan P. ; Hammock, Bruce D. ; Lertora, Juan J L ; Hamm, L. Lee. / Salt loading increases urinary excretion of linoleic acid diols and triols in healthy human subjects. In: Hypertension. 2008 ; Vol. 51, No. 3. pp. 755-761.
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AU - Sigel, Aster

AU - Gill, Rajan S.

AU - Hess, Arthur E.

AU - Cemo, Angela C.

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AB - 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 F1α 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.

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