The effect of arachidonic acid on prostaglandin metabolism in rat isolated perf used kidney

• Published in: The Japanese Journal of Nephrology Vol. 28; no. 6; pp. 777 - 788
• Main Authors: KASAI, YUTAKA, ABE, KEISHI, YOSHINAGA, KAORU, SASO, SHUNICHI
• Format: Journal Article
• Language: Japanese
• Published: Japanese Society of Nephrology 1986
• Subjects: arachidonic acid; perfused kidney; prostaglandins; rat
• ISSN: 0385-2385; 1884-0728
• DOI: 10.14842/jpnjnephrol1959.28.777

The purpose of the present study is to assess the effect of arachidonic acid (AA) and renal perfusion perssure on renal prostaglandin (PG) metabolism. The rat isolated blood-free perfused kidney was used. This system has been proven to be a useful tool for studying the renal hormonal metabolism. In the present study, two different perfusion pressures were employed. We assumed the low perfusion pressure (LPP) as an ischemic state of the kidney expecting the increase in prostacyclin production and the high perfusion pressure (HPP) as a physiological state of the kidney. In high perfusion pressure experiments, AA stimulated the perfusate PGE2, PGF2α secretions biphasically but perfusate 6-keto-PGF1α secretion monophasically. In LPP experiments, perfusate 6-keto-PGF1a increased 6-folds higher than that of HPP experiments. There was no difference in perfusate 6-keto-PGF1α between with AA and without AA experiments in LPP experiments. In HPP experiments, urinary PGE2, PGF2α and thromboxane B2 (TxB2) excretions were stimulated by AA but urinary 6-keto-PGF1α excretion was not stimulated by AA. From these results, the following conclusions were obtained. (a) The prostaglandin metabolisms were different between HPP and LPP experiments. (b) The rat isolated blood-free perfused kidney was able to produce TxB2 and excrete it. (c) 6-keto-PGF1α showed the different releasing pattern from that of PGE2, PGF2α and TxB2 suggesting different metabolic site and/or releasing mechanism.