Changes in Inducible Nitric Oxide Synthase Expression in Experimental Glomerulonephritis

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Abstract
We assessed changes in transcriptional activation of the inducible isoform of nitric oxide synthase (iNOS) in a model of macrophage-dependent proliferative glomerulonephritis in the rat resembling human forms of rapidly progressive nephritis. By the use of a cDNA probe derived from rat glomerular RNA and an RNase protection assay, iNOS expression was assessed at early and late stages of the disease and was correlated with the extent of macrophage infiltration. Prominent iNOS expression occurred in isolated glomeruli 24 hr after onset of immune injury when marked glomerular infiltration by macrophages also occurred. Treatment of animals with immune injury with the arachidonic acid cyclooxygenase inhibitor, indomethacin, potentiated iNOS expression. iNOS expression was short-lived; it was markedly reduced on Day 2 of injury and undetectable on Days 4 and 10, despite sustained infiltration of glomeruli by macrophages. These observations suggest that in glomerular immune injury the enhanced expression of iNOS is not sustainable possibly due to downregulatory factors generated in the course of injury.

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