Rosenblatt S G, Patak R V, Lifschitz M D
Am J Physiol. 1978 Nov;235(5):F473-9. doi: 10.1152/ajprenal.1978.235.5.F473.
Urinary prostaglandin E (PGE) has been utilized as an index of renal PGE production. Recent studies, however, have suggested that the organic acid secretory pathway is a major determinant of endogenous UPGEV (urinary excretion of PGE). The following experiments were designed to quantitatively test this latter view. In clearance studies the administration of para-aminohippurate (PAH) or probenecid (25 mg/kg) failed to alter endogenous UPGEV although PAH clearance fell with probenecid. Comparison of the excretion patterns of exogenously administered [3H]PGE and [14C]inulin after intra-arterial injection into the dog renal artery (Chinard technique) demonstrated both glomerular filtration and secretion of [3H]PGE. Blockade of the organic acid pathway by probenecid (25 mg/kg) abolished [3H]PGE secretion. Indomethacin (1 mg/kg) did not alter the secretion pattern of [3H]PGE, but decreased endogenous UPGEV by over 80%. Because this low dose of indomethacin did not decrease [3H]PGE secretion, it probably decreased endogenous UPGEV by inhibiting synthesis. Thus, these tracer studies do indeed confirm the suggestion that PGE may be excreted by the organic acid pathway. However, the failure of total endogenous UPGEV to fall after blockade of the organic acid pathway would suggest that the component of UPGEV due to this mechanism is quantitatively insignificant.
尿前列腺素E（PGE）已被用作肾脏PGE生成的指标。然而，最近的研究表明，有机酸分泌途径是内源性尿PGE排泄量（UPGEV）的主要决定因素。以下实验旨在定量验证后一种观点。在清除率研究中，尽管给予丙磺舒后对氨基马尿酸（PAH）清除率下降，但给予PAH或丙磺舒（25mg/kg）未能改变内源性UPGEV。经犬肾动脉动脉内注射（Chinard技术）后，比较外源性给予的[3H]PGE和[14C]菊粉的排泄模式，结果表明[3H]PGE既有肾小球滤过又有分泌。丙磺舒（25mg/kg）阻断有机酸途径后消除了[3H]PGE的分泌。吲哚美辛（1mg/kg）未改变[3H]PGE的分泌模式，但使内源性UPGEV降低了80%以上。由于这种低剂量的吲哚美辛并未降低[3H]PGE的分泌，它可能是通过抑制合成来降低内源性UPGEV的。因此，这些示踪研究确实证实了PGE可能通过有机酸途径排泄的观点。然而，阻断有机酸途径后内源性UPGEV总量并未下降，这表明由该机制导致的UPGEV部分在数量上并不重要。
