PGE2, 6-O-PGF1 alpha and sodium balance in essential hypertensive patients.
Insufficient production of PGE2 has been thought to be a pathogenic factor in hypertensive patients on salt loading. However, the inter-relationship between PGE2 and sodium is still uncertain. Essential hypertensive patients participated in a salt balance study for two consecutive 5-day periods of restriction and repletion. Urinary PGE2 increased on the second or the third day of salt balance, but subsequently declined and remained stable. On the fifth day, PGE2 excretion on salt loading was lower than on salt deprivation. Changes in urinary PGE2 during salt loading paralleled those in urinary sodium excretion. Urinary 6-O-PGF1 alpha did not show any significant change. On salt deprivation PGE2 excretion was correlated with plasma renin activity (PRA). These results suggest the possibility that PGE2 is involved in sodium excretion on salt loading and that on salt depletion PGE2 excretion increases in association with activation of the renin-angiotensin axis.
D015121:6-Ketoprostaglandin F1 alpha / Q000652:urine*; D000328:Adult; D015232:Dinoprostone; D005260:Female; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009318:Natriuresis; D011458:Prostaglandins E / Q000652:urine*; D012083:Renin / Q000097:blood; D012964:Sodium / Q000008:administration & dosage / Q000378:metabolism* / Q000652:urine
D011458:Prostaglandins E; D015121:6-Ketoprostaglandin F1 alpha; D012964:Sodium; D012083:Renin; D015232:Dinoprostone