The role of nitric oxide in experimental glomerulonephritis

In recent years, nitric oxide (NO) has been identified as an effector molecule with multiple biological functions. NO production is physiologically involved in the regulation of vascular tone, platelet aggregation and hormone release, in neurotransmission, and in immune defense against several pathogens. However, uncontrolled up-regulation of NO release by cytokine-inducible NO synthases (iNOSs) may cause tissue damage in immune-mediated diseases. In experimental glomerulonephritis, there is now good evidence that glomerular induction of NO synthesis mediates glomerular cell injury. In contrast, an intact constitutive NO release within the glomerular vasculature may be protective by decreasing glomerular capillary pressure. This review discusses the pathophysiological role of NO in glomerulonephritis based on experimental data and provides a perspective for potential anti-inflammatory treatment approaches selectively targeting iNOS overexpression.