Urinary Excretion of 6-Keto-Pgf1_α, TxB₂, and PGE₂ in Pregnancy-Induced Hypertension and Preeclampsia

Abstract

Objective: Our intention was to investigate whether, in pregnancy-induced hypertension (PIH), preeclampsia is accompanied by an altered urinary excretion of 6-keto-PGF1_α (a metabolite of prostacyclin PGI₂), TxB₂ (a metabolite of thromboxane A₂) and PGE₂.

Methods: Our study included 59 PIH patients with a blood pressure > 140/90 mm Hg. Of them, 18 displayed a proteinuria > 300 mg/L and were classified as preeclamptic. As controls, 53 normotensive pregnancies were investigated. Urine samples were purified by solid-phase extraction and reversed-phase HPLC, and 6-keto-PGF_1α TxB₂, and PGE₂ were quantified by radioimmunoassays.

Results: Urinary excretion of vasodilatory prostaglandins in the third trimester was significantly reduced in hypertensive pregnancies compared to controls. Further reductions were observed in preeclamptic patients. Mean values > SEM are: 6-keto-PGF_α: controls 926 ± 49 pg/mg creatinine (crea), PIH 694 ± 49 pg/mg crea, 0.01 < P < 0.001, preeclampsia 424 ± 65 pg/mg crea, P < 0.001; PGE₂: controls 635 ± 34 pg/mg crea, PIH 489 ± 34 pg/mg crea, 0.01 < P < 0.001, preeclampsia 374 ± 28 pg/mg crea, P < 0.001). No significant differences were found in TxB₂ output (controls 300 ± 17 pg/mg crea, PIH 243 ± 14 pg/mg crea, preeclampsia 213 ± 17 pg/mg crea).

Conclusions: We conclude that hypertensive pregnancy disorders do reduce the production of vasodilatory PGI₂ and PGE₂. Thus, the balance between vasodilating and vasoconstrictive prostaglandins was disturbed by a smaller production of PGI₂ and PGE₂ rather than an overproduction of TxA₂. The degree of imbalance correlated with the severity of the disease.

Key Words:

• Kidney
• Preeclampsia
• Pregnancy-induced hypertension
• Prostaglandins
• Urine