AJP - Renal Physiology, Vol 248, Issue 5 698-F704, Copyright © 1985 by American Physiological Society
Prostaglandin inhibitors alter loop segment chloride uptake during furosemide diuresis
K. A. Kirchner
Prostaglandin synthesis inhibition antagonizes the chloruretic effect of
furosemide. To identify the site of this interaction, cortical
micropuncture was performed in furosemide-treated rats during meclofenamate
or indomethacin infusion. Control rats received the vehicle for
prostaglandin synthesis inhibition. The fractional excretion of chloride
decreased from 10.6 +/- 1.0% in control rats to 6.5 +/- 0.93% in
indomethacin-treated rats (P less than 0.01) and to 5.7 +/- 0.7% in
meclofenamate-treated rats (P less than 0.001). Mean arterial pressure,
inulin clearance, renal blood flow, and single nephron glomerular
filtration rate were not different among the groups. Chloride delivery out
of the late proximal tubule was also not different among the groups. Early
distal tubule chloride delivery was greater (P less than 0.001) in control
rats than in either prostaglandin-inhibited group. Late distal chloride
delivery was also greater in control rats. Calculated loop segment chloride
uptake was 9 +/- 2% in furosemide-treated control rats but 18 +/- 2% in
both indomethacin- and meclofenamate-treated rats (P less than 0.05).
Distal tubule chloride uptake was greater in control than in
prostaglandin-inhibited rats. Thus, the attenuated chloruretic response to
furosemide observed in indomethacin- or meclofenamate-treated animals may
in part result from increased chloride uptake in the loop segment of
superficial nephrons.
