VASOPRESSIN RELEASE DURING ENDOTOXEMIC SHOCK IN MICE LACKING INDUCIBLE NITRIC OXIDE SYNTHASE

• Published in: The FASEB journal 2006-03, Vol.20 (5), p.A1445-A1446
• Main Authors: Carnio, Evelin C, Batalhao, Marcelo E., Stabile, Angelita M.
• Format: Article
• Language: English
• ISSN: 0892-6638; 1530-6860
• DOI: 10.1096/fasebj.20.5.A1445-d

We have tested the hypothesis that nitric oxide (NO) arising from inducible nitric oxide synthase (iNOS) is responsible for the deficiency in vasopressin release and consequent hypotension during endotoxemic shock. Wild–type (WT) and iNOS knockout mice (KO−/− mice) were intravenously injected with either saline or Escherichia coli lipopolysaccharide (LPS) 1.0 mg/kg in a final volume of 0.03 ml. Mean arterial blood pressure (MAP) was measured and vasopressin (AVP) plasma levels determined before and after LPS or saline injection. In WT mice we found a significant drop in MAP after two hours of LPS administration, which lasted low until the end of the sixth hour of experiment. We also observed an increase in AVP plasma levels at the second and fourth hour of experiment, returning thereafter to basal levels. Conversely LPS injection in iNOS KO mice elicited sustained increase in plasma AVP concentration, and attenuation of the fall in blood pressure. These data indicate that NO arising from the iNOS plays an important inhibitory role in AVP release during endotoxemia and may be responsible for the hypotension occurring during this vasodilatory shock.