Nitric oxide and glomerulonephritis.
The normal glomerulus expresses constitutive nitric oxide (NO) synthesis. Increased NO from inducible nitric oxide synthase (iNOS) occurs in acute immune glomerulonephritis (GN), in which rapid induction probably depends on local cytokines and/or oxygen radical production. Although intrinsic glomerular cells possess iNOS, in acute GN, a leukocyte origin for iNOS activity is most evident. Although NO potentially could be toxic or protective, there is as yet no clear understanding of how it affects the pathogenesis of GN. This may depend on the amount present, which in turn depends on NOS gene regulation, simultaneous production of other radicals, and the activity of arginase. High-output NO has been implicated in injury in only one model of GN, and no effect of iNOS knockout found in another. The concept is emerging that constitutive NO is critical for offsetting increased vasoconstriction in the injured glomerulus.
Cattell
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Department of Histopathology, St. Mary's Hospital Medical School, London.
D000818:Animals; D001120:Arginine / Q000378:metabolism; D005921:Glomerulonephritis / Q000209:etiology*; D006801:Humans; D008070:Lipopolysaccharides / Q000633:toxicity; D008181:Lupus Nephritis / Q000209:etiology; D051379:Mice; D018345:Mice, Knockout; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000502:physiology; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III
D008070:Lipopolysaccharides; D009569:Nitric Oxide; D001120:Arginine; C496319:NOS2 protein, human; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496317:Nos2 protein, mouse; C496315:Nos3 protein, mouse