Dependence of pulmonary prostaglandin metabolism on carrier-mediated transport processes

¹ Department of Ophthalmology, College of Physicians and Surgeons, Columbia University, New York City 10032

Inhibitors of prostaglandin (PG) transport (probenecid, indomethacin, or bromcresol green) were found to eliminate the difference between the pulmonary transit time of ³H and ¹⁴C when [³H]PGF₂ and [¹⁴C]sucrose were injected as a single intra-arterial bolus into the isolated perfused rat lung. Similar results were obtained with PGE₁. The transit time of [³H]PGA₁ was not significantly different from that of [¹⁴C]sucrose even in the absence of an inhibitor. These inhibitors increased the amount of [³H]PGF₂ or [³H]PGE₁ and decreased the amount of [³H]PG metabolites found in the venous effluent; these agents also inhibited the pulmonary metabolism of continuously infused, nonradioactive PGF₂. One of the three inhibitors, bromcresol green, was shown not to be an effective inhibitor of PG metabolism in cell-free preparations of rat lung homogenates. These results indicated that under normal conditions, PG's are rapidly transported into intracellular compartment(s) where they are metabolized. Inhibition of this transport process prevents rapid access of PG's to the cytoplasmic enzymes and therefore inhibits pulmonary PG metabolism. This implies that inhibitors of PG transport, including anti-inflammatory organic acids, and some PG antagonists, metabolites, and analogues, can be expected to inhibit the pulmonary metabolism of PG's, and thus could potentiate the systemic effects of endogenous or exogenous PG's.

Submitted on June 3, 1976

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