ESSENTIAL FATTY-ACID DEFICIENCY IMPAIRS THE RESPONSIVENESS OF RENAL PELVIC SENSORY RECEPTORS

The role of prostaglandins in renal sensory receptor activation was ex amined in rats fed an essential fatty acid-deficient (EFAD) diet to ca use tissue arachidonate depletion. Littermates fed a standard diet wer e used as controls. In anesthetized rats, the increases in afferent re nal nerve activity due to increasing ureteral pressure 2.5, 5, 7.5, 10 , 12.5, and 15 mmHg were significantly reduced by the EFAD diet (P < 0 .02): 3 +/- 5, 3 +/- 5, 11 +/- 5, 9 +/- 5, 19 +/- 3, and 17 +/- 5%, re spectively, in EFAD rats and 23 +/- 11, 36 +/- 15, 50 +/- 15, 52 +/- 8 , 72 +/- 17, and 90 +/- 19%, respectively, in control rats. In EFAD ra ts, addition of prostaglandin E(2) (PGE(2)) to the renal pelvic perfus ate restored the afferent renal nerve activity response to increased u reteral pressure toward that in control rats. PGE(2) had no effect in control rats. Also the afferent renal nerve activity responses to rena l pelvic perfusion with bradykinin at 4, 20, 100, and 500 mu g/ml were significantly suppressed by the EFAD diet (P < 0.01): 13 +/- 15, 5 +/ - 7, 60 +/- 19, and 63 +/- 20%, respectively, in EFAD rats and 122 +/- 23, 142 +/- 31, 172 +/- 19, and 190 +/- 39%, respectively, in control rats. These results demonstrate an important role for arachidonate me tabolites, particularly PGE(2), in renal sensory receptor activation. Together with our previous studies showing that indomethacin blocks th e afferent renal nerve activity responses to increased ureteral pressu re or bradykinin, the present studies provide strong evidence for an e ssential role of prostaglandins in renal sensory receptor activation.