Effects of inhibition of prostaglandin-synthesis on renal electrolyte excretion and concentrating ability in healthy man.
In five healthy subjects inhibition of prostaglandin (PG)-synthesis with indomethacin did not significantly alter glomerular filtration, urinary flow rate or sodium and potassium excretion during control urine collection periods or i.v. hypertonic saline infusion. Saline administration was accompanied by a fall in urinary PGEI-excretion from 0.58 +/- 0.14 to 0.26 +/- 0.09 ng/min (p less than 0.05). While indomethacin had no effect on basal urinary osmolality (Uosm), renal concentrating ability following hypertonic saline or i.v. administration of 100 mU lysine-vasopressin significantly increased in the presence of indomethacin with Uosm rising from 805 +/- 25 to 970 +/- 53 mosm/L (p less than 0.01) and from 839 +/- 47 to 996 +/- 62 mosm/L (p less than 0.01), resp. Since this was not accompanied by respective changes in urinary excretion of cyclic adenosine monophosphate (cAMP) mechanisms other than PG-antagonism of vasopressin, such as decreased medullary washout of solute, may contribute to enhanced renal concentrating ability following inhibition of PG-synthesis with indomethacin.
D000328:Adult; D000242:Cyclic AMP / Q000652:urine; D016861:Cyclooxygenase Inhibitors; D004231:Diuresis / Q000187:drug effects; D004573:Electrolytes / Q000652:urine*; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects / Q000378:metabolism*; D007671:Kidney Concentrating Ability / Q000187:drug effects*; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D011188:Potassium / Q000652:urine; D011458:Prostaglandins E / Q000652:urine
D016861:Cyclooxygenase Inhibitors; D004573:Electrolytes; D011458:Prostaglandins E; D000242:Cyclic AMP; D011188:Potassium; D007213:Indomethacin