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Vasopressin release during endotoxemic shock in mice lacking inducible nitric oxide synthase
Author(s) -
Carnio E.C.
Publication year - 2005
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/j.clpt.2004.11.038
Subject(s) - vasopressin , nitric oxide synthase , lipopolysaccharide , nitric oxide , endocrinology , mean arterial pressure , medicine , septic shock , shock (circulatory) , blood pressure , chemistry , arginine , pharmacology , sepsis , biochemistry , heart rate , amino acid
Background 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. Methods and results Wild‐type (WT) and iNOS knockout mice (KO) 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 injection. In WT mice we found a significant drop in MAP after LPS administration, which lasted low until the end of the experiment. We also observed an increase in AVP plasma levels at the second hour of experiment, returning thereafter to basal levels. Conversely LPS injection in iNOS KO mice elicited sustained increase in plasma AVP concentration and maintenance of the blood pressure. Conclusion 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. Clinical Pharmacology & Therapeutics (2005) 77 , P9–P9; doi: 10.1016/j.clpt.2004.11.038