Role of nitric oxide in a toxin-induced model of haemolytic uraemic syndrome |
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Authors: | J. M. Williams C. J. Lote A. Thewles J. A. Wood A. J. Howie M. C. Williams D. A. Adu C. M. Taylor |
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Affiliation: | (1) Renal Research, Clinical Research Block, Queen Elizabeth Hospital, Birmingham, B15 2TH, UK e-mail: J.M.Williams.MED@bham.ac.uk Tel.: +44-121-4143785, Fax: +44-121-6272527, GB;(2) Renal Research, University Hospital, Birmingham, UK, GB;(3) Department of Physiology, University of Birmingham, UK, GB;(4) Department of Pathology, University of Birmingham, UK, GB;(5) Department of Nephrology, The Birmingham Children’s Hospital, Birmingham, UK, GB |
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Abstract: | The role of nitric oxide in the pathogenesis of glomerular thrombotic microangiopathy was explored using an established rat model in which ricin with or without lipopolysaccharide induced glomerular thrombosis. Ricin alone caused a small rise in the plasma concentration of nitric oxide (control 9.2+/-0.7 microM, ricin 23.3+/-6.3 microM at 7 h). This increase occurred after the development of glomerular thrombosis. Nitric oxide synthase (NOS) activity in the kidney showed no significant change from control values (control 5.66+/-2.7 pmol/min per ml homogenate, ricin 7.52+/-1.8 pmol/min per ml homogenate, total activity). When ricin and lipopolysaccharide were administered together, calcium-independent NOS activity increased whereas calcium-dependent activity decreased (1.22+/-2.6 pmol/min per ml homogenate). The increase in calcium-independent NOS activity correlated with a high plasma concentration of interleukin-1beta in the ricin plus lipopolysaccharide group (4,036.83+/-1,001.5 pg/ml). These data indicate that thrombus formation in a rat model of haemolytic uraemic syndrome is independent of the effects of nitric oxide. |
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Keywords: | Haemolytic uraemic syndrome Ricin Verocytotoxin Nitric oxide Cytokines Glomerular thrombosis |
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