AJP - Regulatory, Integrative and Comparative Physiology, Vol 268, Issue 1 164-R170, Copyright © 1995 by American Physiological Society
Essential fatty acid deficiency impairs the responsiveness of renal pelvic sensory receptors
U. C. Kopp, D. M. Farley, L. A. Smith and H. R. Knapp
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City.
The role of prostaglandins in renal sensory receptor activation was
examined in rats fed an essential fatty acid-deficient (EFAD) diet to cause
tissue arachidonate depletion. Littermates fed a standard diet were used as
controls. In anesthetized rats, the increases in afferent renal 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%, respectively, in EFAD
rats and 23 +/- 11, 36 +/- 15, 50 +/- 15, 52 +/- 8, 72 +/- 17, and 90 +/-
19%, respectively, in control rats. In EFAD rats, addition of prostaglandin
E2 (PGE2) to the renal pelvic perfusate restored the afferent renal nerve
activity response to increased ureteral pressure toward that in control
rats. PGE2 had no effect in control rats. Also the afferent renal nerve
activity responses to renal pelvic perfusion with bradykinin at 4, 20, 100,
and 500 micrograms/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 metabolites, particularly PGE2, in renal sensory receptor
activation. Together with our previous studies showing that indomethacin
blocks the afferent renal nerve activity responses to increased ureteral
pressure or bradykinin, the present studies provide strong evidence for an
essential role of prostaglandins in renal sensory receptor activation.
