Increment of prostaglandin E2 in association with elevation of urinary sodium excretion following lead administration

Toxicol Lett. 1986 Sep;32(3):221-6. doi: 10.1016/0378-4274(86)90111-6.

Abstract

Lead administered to semi-fasted rats caused an elevation of urinary sodium excretion but no increase of urinary potassium excretion as previously observed in fasted rats. Moreover, in this experiment it was found that urinary and serum prostaglandin E2 (PG E2) contents were increased in association with the elevation of urinary sodium excretion by lead and that natriuresis was suppressed by indomethacine treatment. These findings suggest a stimulation of prostaglandin synthetase rather than to a suppression of the renin-angiotensin-aldosterone system as a primary reaction caused by the lead administration.

MeSH terms

  • Administration, Oral
  • Aldosterone / blood
  • Animals
  • Cyclooxygenase Inhibitors*
  • Dinoprostone
  • Drug Interactions
  • Ethylene Glycols / pharmacology
  • Food Deprivation
  • Indomethacin / pharmacology
  • Injections, Intraperitoneal
  • Kidney Cortex / drug effects
  • Kidney Cortex / metabolism
  • Lead / toxicity*
  • Male
  • Potassium / urine
  • Prostaglandin-Endoperoxide Synthases / metabolism
  • Prostaglandins E / metabolism*
  • Rats
  • Rats, Inbred Strains
  • Renin / blood
  • Sodium / urine*
  • Sodium-Potassium-Exchanging ATPase / metabolism

Substances

  • Cyclooxygenase Inhibitors
  • Ethylene Glycols
  • Prostaglandins E
  • Lead
  • Aldosterone
  • Sodium
  • Prostaglandin-Endoperoxide Synthases
  • Renin
  • Sodium-Potassium-Exchanging ATPase
  • methyl cellosolve
  • Dinoprostone
  • Potassium
  • Indomethacin