Studies of the effects of essential fatty acid deficiency in the rat

Abstract

We report a model of prostaglandin depletion induced in rats by fasting for 11 days, followed by institution of an essential fatty acid-deficient diet. Urinary prostaglandin E, 2 weeks after this diet had been implemented, was 22 ± 2 ng/24 hours compared to 113 ± 8.5 ng/24 hours in controls (P < 0.01). There was no difference in 24-hour urine volume or solute excretion in controls and essential fatty acid-deficient rats. Five hours after administration of NaCl, 10 mM/kg, essential fatty acid-deficient diet rats excreted 1,85 ± 0.78 ml urine compared to 6.42 ± 2.26 ml in control (p < 0.01) with Na+ excretion 447 ± 273 μEq in essential fatty acid-deficient rats vs 1483 ± 366 μEq in control (P < 0.01). Intravenous isotonic NaCl, 1.5% body weight, resulted in increased urine flow rate in control rats from 8.3 ± 2 μl/min to 28.7 ± 8.8 μl/min, with sodium excretion increasing from 0.19 ± 0.2 to 3.3 ± 0.9 μEq/min. In the essential fatty acid-deficient diet animals, there was no significant change in flow rate, 6.07 ± 2.43 to 9.85 ± 4.29 μl/min, or sodium excretion, 0.09 ± 0.03 to 0.40 ± 0.24 μEq, after saline infusion. There was no difference in the glomerular filtration rate or plasma aldosterone in the two groups after the salt load. When given a water load, 3 ml/100 g body weight, essential fatty acid-deficient diet rats excreted 2.5 ± 0.7 ml in 5 hours compared to 6.3 ± 1.4 ml in controls (P < 0.01). The defect in water excretion was not due to increased sensitivity to antidiuretic hormone, since similar sensitivity to this hormone was demonstrated in the essential fatty-acid-deficient diet and control rats during a water diuresis. When isotonic saline was substituted for drinking water, there was an increase in systolic blood pressure in essential fatty acid-deficient diet rats from 124 ± 2 to 142 ± 3 mm Hg over 9 days (P < 0.01) compared to 122 ± 2 before and 122 ± 2 mm Hg after saline drinking in controls. The administration of linoleic acid for 4 days increased urinary prostaglandin E excretion to 114 ± 15 ng/24 hours from 23 ± 4 (P < 0.01), and the alterations in the ability to excrete a sodium and water load were reversed. In essential fatty acid-deficient diet animals made hypertensive by 9 days of saline drinking, the institution of linoleic acid to the diet normalized the blood pressure despite the continued administration of saline. These studies demonstrate fatty acid-deficient diet animals develop salt-sensitive hypertension with a combined defect in both sodium and water excretion which is reversed following correction of the essential fatty acid deficiency.