Abstract
An investigation was carried out to determine whether or not the administration of indomethacin to Li-treated rats would raise PLi2, and whether or not there would be any change in the type or severity of Li-induced renal functional abnormalities. It was found that indomethacin increased PLi, apparently by decreasing CLi. Umax, already reduced by Li, was further impaired by the additional administration of indomethacin. The Li-induced impairment of TcH2O was not worsened by added indomethacin, but a wide variance of the data might have masked any effect. Significant inverse correlations were found between Umax and PLi and between maximum TcH2O and PLi, suggesting that the indomethacin-induced impairment in renal concentrating capacity is attributable to the increased PLi.
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