Diminished Urinary Prostacyclin Metabolite in Essential Hypertension

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Abstract
1. Urinary excretion rate of 6-keto-prostaglandin F1α (6-keto-PGF1α), a stable non-enzymatic transformation product of prostacyclin (PGI2), was measured in 13 patients with sustained essential hypertension and in nine normotensive control subjects by a specific radioimmunoassay. 2. Patients with essential hypertension had significantly lower 6-keto-PGF1α excretion rates irrespective of their sex, but in both groups urinary 6-keto-PGF1α was lower in females. 3. Sodium excretion was significantly correlated with urinary 6-keto-PGF1α only in hypertensive subjects. There was also a positive correlation between 6-keto-PGF1α and urine volume in control subjects and in hypertensive patients. 4. If diminished urinary 6-keto-PGF1α reflects suppressed endogenous PGI2 production, a deficiency in this important vasodepressor substance in essential hypertension may contribute to the pathogenesis of this disease.

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