QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hansen, H. S. Articles by Jensen, B. Search for Related Content PubMed PubMed Citation Articles by Hansen, H. S. Articles by Jensen, B.

Urinary Excretion of Arginine-Vasopressin and Prostaglandin E₂ in Essential Fatty Acid-Deficient Rats after Oral Supplementation with Unsaturated Fatty Acid Esters¹

Biochemical Laboratory, Royal Danish School of Pharmacy, Universitetsparken 2, 2100 Copenhagen Ø, Denmark

Essential fatty acid-deficient rats were supplemented with 300 mg/d of pure fatty acid esters: oleate (O), linoleate (L), arachidonate (A), and columbinate (C) for 10 d. The 24-h urine collections from each animal, collected 3 d before supplementations and again the last 3 d of the 10-d supplementation period, were analyzed for volume, and by radioimmunoassay for arginine-vasopressin (AVP) and prostaglandin E₂ (PGE₂). Linoleate and arachidonate supplements both decreased the initial high urinary AVP excretion, whereas it was further increased by the oleate supplement. There was no effect of columbinate supplementation on urinary AVP excretion. Urinary PGE₂ excretion was increased ca. twofold by both linoleate and oleate supplements, increased ca. fivefold by arachidonate supplementation but was unaffected by columbinate supplementation. There was no effect of any of the supplemented fatty acids on urine output. Fatty acid analysis of total kidney lipids revealed a low percentage of 20:3(n-9) in the rats supplemented with (n-6) fatty acid (L, A and C). The triene-tetraene ratio was 1.8 ± 0.6 (n = 6) in the kidneys of the oleate-supplemented rats. No relationship was found between urinary PGE₂ excretion and the percentage of arachidonate or the ratio of 20:3 (n-9)/20:4(n-6) in total kidney lipids. It is suggested that increased urinary AVP excretion in EFA-deficient rats is mainly caused by a change in the renal excretatory mechanism of AVP rather than reflecting an increased plasma AVP concentration. Furthermore it is suggested that renal PGE₂ synthesis in vivo is unaffected by high levels of 20:3(n-9) in kidney lipids.

KEY WORDS: • columbinic acid • linoleic acid • arachidonic acid • urine output

¹ This work has been supported by the Danish Medical Research Council (J. no. 12-4175, 12-4449, 12-4950, and 1981-360-9).

Manuscript received 21 June 1985. Revision accepted 14 October 1985.