356 SALT LOADING INCREASES THE URINARY EXCRETION OF LINOLEIC DIOLS AND TRIOLS IN HEALTHY HUMAN SUBJECTS.

Background/Aims Hypertension has been associated with disturbed membrane function. Changes in membrane composition related to increased dietary intake of the polyunsaturated fatty acid linoleic acid (LOA) have been shown in clinical studies to increase red blood cell membrane LOA fraction, reduce systolic blood pressure, alter red blood cell and white blood cell sodium transport processes, and increase prostaglandin production and sodium excretion. We studied the effect of salt loading on the excretion of linoleic acid diols and triols to determine if oxidative LOA metabolism is associated with salt handling by the kidney in human subjects. Methods Twelve healthy subjects were recruited from the New Orleans population (pre-Katrina) and admitted to Tulane-LSU Charity Hospital GCRC after a 5-day outpatient lead in phase on a 160 mmol sodium (Na) diet. On inpatient day 1 (D1), the subjects were maintained on the 160 mmol Na diet and 24-hour urine was collected for the LOA diols and triols: 9,10-DiHOME, 12,13-DiHOME, 9,10,13-TriHOME, and 9,12,13-TriHOME. On day 2 (D2), the subjects received 2 L of normal saline IV over 4 hours and continued on 160 Na mmol diet (total 460 mmol Na). Two 12-hour urine collections were obtained. On day 3, the patient received three 40 mg oral doses of furosemide and two 12-hour urine collections were obtained, and the patient was given a 10 mmol Na diet. The urinary LOA metabolites were measured by HPLC-tandem quadrapule mass spectroscopy at UC-Davis. Repeated measures ANOVA with a Tukey test was used to compare LOA metabolite levels during salt-loaded and salt-depleted periods. Results The urinary excretion of all LOA diols and triols measured increased significantly three- to fivefold during the day of the intravenous salt loading (D2) when the compared with the salt-depleted periods and D1. Conclusions Salt loading stimulates the renal production of LOA diols and triols, which may inhibit tubular sodium reabsorption, thereby assisting the excretion of the sodium load.