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J Appl Physiol (January 31, 2003). doi:10.1152/japplphysiol.01042.2002
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Submitted on November 14, 2002
Accepted on January 30, 2003

Differential role of nitric oxide synthase isoforms in fever of different etiologies: studies using NOS gene deficient mice

Wieslaw Kozak1 and Anna Kozak2*

1 Department of Physiology, Medical College of Georgia, Augusta, GA, USA; Institute of General and Molecular Biology, Department of Immunology, University of Nicolaus Copernicus, Torun, Poland
2 Department of Physiology, Medical College of Georgia, Augusta, GA, USA

* To whom correspondence should be addressed. E-mail: akozak{at}mail.mcg.edu.

Male C57BL/6J mice deficient in nitric oxide synthase (NOS) genes (knockout; KO) and control (wild-type) mice were implanted intra-abdominally with battery operated miniature biotelemeters (model VMFH MiniMitter, Sunriver, OR) to monitor changes in body temperature. Intravenous injection of lipopolysaccharide (LPS; 50 µg/kg) was used to trigger fever in response to systemic inflammation in mice. To induce a febrile response to localized inflammation, the mice were injected subcutaneously with pure turpentine oil (30 µl/animal) into the left hind limb. Oral administration (gavage) of L-NMMA for three days (80 mg/kg/day in corn oil) prior to injection of pyrogens was used to inhibit all three nitric oxide synthases (D-NMMA and corn oil were used as control). In normal male C57BL/6J mice, L-NMMA inhibited the LPS-induced fever by ca. 60%, whereas it augmented fever by ca. 65% in mice injected with turpentine. Challenging the respective NOS KO mice with LPS and with L-NMMA revealed that inducible (iNOS) and neuronal (nNOS) isoforms are responsible for the induction of fever to LPS whereas endothelial (eNOS) is not involved. In contrast, none of the NOS isforms appeared to trigger fever to turpentine. Inhibition of eNOS, however, exacerbates fever in mice treated with L-NMMA and turpentine, indicating that eNOS participates in the antipyretic mechanism. These data support the hypothesis that nitric oxide is a regulator of fever. Its action differs, however, depending on the pyrogen used and the nitric oxide synthase isoform.




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