Further studies on the effects of cyclooxygenase inhibitors on compensatory renal growth.
The primary stimulus for compensatory renal growth is unknown. This process may be regulated by a circulating renotropic factor or may reflect a growth response to increased work. Prostaglandins appear to participate in compensatory renal growth as indomethacin has been shown to attenuate increases in both renal mass and function after uninephrectomy in rats. The goal of the present study was to test the effects of other cyclooxygenase inhibitors on compensatory renal growth and to evaluate the effects of indomethacin on renal growth in vitro in response to the purported renotropic factor. Both ibuprofen and meclofenamate retarded compensatory renal growth two days after uninephrectomy in rats (p less than 0.05). The addition of indomethacin to the medium of kidney slices incubating with sera from uninephrectomized rats reduced renal DNA synthesis, whereas indomethacin had no effect on renal growth when added to slices incubating with sera from intact animals. These data provide more support for an important role for prostaglandins in compensatory renal growth.
D000818:Animals; D016861:Cyclooxygenase Inhibitors; D004247:DNA / Q000096:biosynthesis; D007052:Ibuprofen / Q000494:pharmacology*; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects / Q000254:growth & development*; D008297:Male; D008469:Meclofenamic Acid / Q000494:pharmacology*; D009392:Nephrectomy; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D062367:ortho-Aminobenzoates / Q000494:pharmacology*
D016861:Cyclooxygenase Inhibitors; D062367:ortho-Aminobenzoates; D008469:Meclofenamic Acid; D004247:DNA; D007052:Ibuprofen; D007213:Indomethacin