6-ketoprostaglandin-e1 and Hypertension

Insufficient production of prostaglandins, which are possible antihypertensive agents, may be a pathogenetic factor in hypertensive patients on salt loading. We compared the levels of plasma PGE2, plasma renin activity (PRA) and urinary 6-keto-PGF1 alpha (6-O-PGF1 alpha), a major stable metabolite of PGI2, on day 5 of salt deprivation and also on day 5 of subsequent salt loading in 17 patients with essential hypertension. Salt loading decreased plasma PGE2, and slightly increased urinary 6-O-PGF1 alpha. On salt loading, a positive correlation was found between the levels of plasma PGE2 and urinary sodium excretion. On salt deprivation, PRA was significantly correlated with plasma PGE2. The per cent change in mean blood pressure on changing from salt restriction to salt loading was inversely correlated with the per cent change in PGE2, and positively correlated with the per cent change in 6-O-PGF1 alpha excretion. These findings suggest that on salt restriction, PGE2 is involved in the renin-angiotension system and that on salt loading, PGE2 is produced to compensate for the excessive sodium. The finding that PGE2 production was attenuated progressively as the mean blood pressure increased on salt loading in patients with essential hypertension suggests that insufficient compensatory PGE2 production is a pathogenetic factor in salt-induced hypertensive patients. In contrast, PGI2 may be produced adaptively to regulate blood pressure during changes in salt balance.

Topics: Adult; Aged; Alprostadil; Blood Pressure; Diet, Sodium-Restricted; Dinoprostone; Epoprostenol; Female; Humans; Hypertension; Male; Middle Aged; Prostaglandins E; Radioimmunoassay; Renin; Sodium; Sodium Chloride

Patients with pregnancy-induced hypertension have higher prostaglandin (PG) F concentrations in radial arterial blood (0.39 +/- 0.03 ng/ml) than control subjects (0.24 +/- 0.03 ng/ml) and higher (PGE plus PGF) concentrations in uterine venous blood obtained at the time of cesarean section (1.62 +/- 0.18 versus 1.03 +/- 0.12 ng/ml in the control group). The present results suggest that both PGE and PGF production by the uterus in patients with pregnancy-induced hypertension is increased but that catabolism of PGF by the lung is compromised; this permits larger quantities of the vasoconstrictor PG to pass into the systemic circulation, where it may cause hypertension directly or indirectly, by association with other vasoactive substances.

Topics: Alprostadil; Arteries; Cesarean Section; Female; Humans; Hypertension; Labor, Obstetric; Lung; Placenta; Pregnancy; Pregnancy Complications, Cardiovascular; Prostaglandins E; Prostaglandins F; Uterus; Veins