Increment of prostaglandin E2 in association with elevation of urinary sodium excretion following lead administration.
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.
D000284:Administration, Oral; D000450:Aldosterone / Q000097:blood; D000818:Animals; D016861:Cyclooxygenase Inhibitors; D015232:Dinoprostone; D004347:Drug Interactions; D005026:Ethylene Glycols / Q000494:pharmacology; D005508:Food Deprivation; D007213:Indomethacin / Q000494:pharmacology; D007274:Injections, Intraperitoneal; D007672:Kidney Cortex / Q000187:drug effects / Q000378:metabolism; D007854:Lead / Q000633:toxicity*; D008297:Male; D011188:Potassium / Q000652:urine; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D011458:Prostaglandins E / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012083:Renin / Q000097:blood; D012964:Sodium / Q000652:urine*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D016861:Cyclooxygenase Inhibitors; D005026:Ethylene Glycols; D011458:Prostaglandins E; D007854:Lead; D000450:Aldosterone; D012964:Sodium; D011451:Prostaglandin-Endoperoxide Synthases; D012083:Renin; D000254:Sodium-Potassium-Exchanging ATPase; C005219:methyl cellosolve; D015232:Dinoprostone; D011188:Potassium; D007213:Indomethacin