Abstract

Twenty-four hour urinary 6-keto-PGF1-alpha and TXB 2 excretions were measured in Sprague Dawley rats treated with 100 ppm lead acetate for 12 weeks, then repeated at 14 weeks when lead administration was discontinued. Control animals and lead-treated animals given 0.5% dimercaptosuccinic acid (DMSA) for 2 weeks were compared. Blood leads at 12 weeks averaged 12.4 ± 1.8 μg/dL and at 14 weeks averaged 3.2 ± 0.2 μg/dL in the lead-treated animals compared to <1 μg/dL in the control and DMSA-treated animals. While raising blood pressure, lead administration did not affect either 6-keto-PGF1-alpha or TXB 2 excretion at either 12 or 14 weeks. There was a significant decrease in 6-keto-PGF1-alpha excretion at 14 weeks in the DMSA-treated rats. This effect was probably related to the scavenging of reactive oxygen species by DMSA. Thus, chronic exposure to low levels of lead resulted in sustained hypertension without affecting urinary excretions of 6-keto-PGF1-alpha or TXB 2. This observation suggests that occurrence of lead-induced hypertension under the given conditions in rat may not involve alterations of renal production of vasodilating or vasoconstrictive eicosanoids.

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