1. To examine the hypothesis that the normalcy of blood pressure, despite an increase in circulating angiotensin II, and the blood pressor hyporesponsiveness to infusion of pressor agents which are associated with hypokalaemia, are due to overproduction of prostacyclin, the principal prostaglandin (PG) synthesized by the vascular endothelium, we studied the effect of experimental hypokalaemia on the urinary excretion of immunoreactive 6-keto-prostaglandin F1 alpha, a stable metabolite of prostacyclin, in the rat. 2. The animals were fed on a potassium-deficient diet for 9 days. Twenty-four hour urine samples were collected daily for measurement of urinary excretion of immunoreactive 6-keto-PGF1 alpha, PGE2 and 13,14-dihydro-15-keto-PGF2 alpha (PGFM). 3. Hypokalaemia caused significant increases of the three prostaglandins measured. 4. We conclude that hypokalaemia is a potent stimulus of both renal and vascular prostaglandins. The results suggest that an increase in prostacyclin synthesis in peripheral blood vessel walls may be responsible for the resistance of blood pressure to infusion of pressor substances as well as for the normalcy of blood pressure, despite the presence of high circulating angiotensin II concentrations, in conditions associated with hypokalaemia.
To assess the possible effect upon the fetus of maternal ingestion of the prostaglandin synthetase inhibitor, mefenamic acid, taken during mid-pregnancy (15-22 weeks) to prevent spontaneous abortion, samples of fetal blood were collected at fetoscopy from 13 treated and 14 untreated control cases. Mefenamic acid levels in the fetus were 32-54% of those in the mothers in the treated group, while prostaglandins E2 (PGE2), 6-oxo-PGF1 alpha and PGFM were all slightly but not significantly lower in those patients given 500 mg mefenamic acid 40-180 min prior to sampling than in untreated controls. Results indicate that the prostaglandin synthetase inhibitor crosses the placenta at this early gestation and may possibly suppress fetal prostaglandin production.
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