Sodium intake as a determinant of urinary prostaglandin E2 excretion.
The effect of salt-loading on urinary prostaglandin D2 (PGE2) was studied in the rat. PGE2 doubled after 4 days of gavage with 40 ml 0.9% saline. Control animals receiving 5% glucose or tap water did not show this increase. When rats were allowed ad lib saline, PGE2 increased after 2 weeks, but returned to normal at 5 weeks. This same phenomenon of increased PGE2 early in the course of salt-loading was also observed in Dahl salt-sensitive and salt-resistant rats fed an 8% salt diet. Inhibition of prostaglandin biosynthesis by meclofenamate or indomethacin did not attenuate the natriuretic effect of saline loading. We conclude: 1) Salt-related changes in PGE2 is a time-dependent phenomenon, and 2) PGE2 is not the natriuretic factor since levels normalize despite continued salt-loading, and natriuresis was unaffected by prostaglandin blockade.
D000284:Administration, Oral; D000818:Animals; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D008469:Meclofenamic Acid / Q000494:pharmacology; D011458:Prostaglandins E / Q000652:urine*; D011863:Radioimmunoassay; D051381:Rats; D012964:Sodium / Q000652:urine; D012965:Sodium Chloride / Q000008:administration & dosage / Q000494:pharmacology*
D011458:Prostaglandins E; D012965:Sodium Chloride; D008469:Meclofenamic Acid; D012964:Sodium; D007213:Indomethacin