Renal concentrating defect in the hypokalemic rat is prostaglandin independent
- 1 January 1980
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Renal Physiology
- Vol. 238 (1) , F37-F41
- https://doi.org/10.1152/ajprenal.1980.238.1.f37
Abstract
Rats on a K-deficient (n = 12) and K-supplemented (n = 12) diet underwent a urinary concentrating test before and after prostaglandin [PG] inhibition with indomethacin. The drug did not alter maximal urinary osmolality in normokalemic rats. Likewise, the abnormal maximal urinary osmolality of K-depleted rats was not improved by PG inhibition (1533 .+-. 124 before and 1475 .+-. 88 mosmol/kg H2O after indomethacin). Control animals receiving a blank diluent instead of indomethacin showed no change in maximal concentrating ability between equally timed dehydration tests. Indomethacin caused no significant alterations in blood urea nitrogen or creatinine. Direct measurements of renal medullary PG revealed no difference between K-depleted (22.9 .+-. 4.4 pg/mg) and normokalemic (23.6 .+-. 2.3 pg/mg) rats. Indomethacin significantly and comparably lowered PG content in both K-depleted and normokalemic rats. These studies reveal no enhancement of PG synthesis with K depletion.This publication has 1 reference indexed in Scilit: