Role of neuronal nitric oxide synthase in hypoxia-induced anapyrexia in rats

Citation
Aa. Steiner et al., Role of neuronal nitric oxide synthase in hypoxia-induced anapyrexia in rats, J APP PHYSL, 89(3), 2000, pp. 1131-1136
Citations number
41
Categorie Soggetti
Physiology
Journal title
JOURNAL OF APPLIED PHYSIOLOGY
ISSN journal
87507587 → ACNP
Volume
89
Issue
3
Year of publication
2000
Pages
1131 - 1136
Database
ISI
SICI code
8750-7587(200009)89:3<1131:RONNOS>2.0.ZU;2-1
Abstract
Anapyrexia (a regulated decrease in body temperature) is a response to hypo xia that occurs in organisms ranging from protozoans to mammals, but very l ittle is known about the mechanisms involved. Recently, it has been shown t hat the NO pathway plays a major role in hypoxia-induced anapyrexia. Howeve r, very little is known about which of the three different nitric oxide syn thase isoforms (neuronal, endothelial, or inducible) is involved. The prese nt study was designed to test the hypothesis that neuronal nitric oxide syn thase (nNOS) plays a role in hypoxia-induced anapyrexia. Body core temperat ure (T-c) of awake, unrestrained rats was measured continuously using biote lemetry. Rats were submitted to hypoxia, 7-nitroindazole (7-NI; a selective nNOS inhibitor) injection, or both treatments together. Control animals re ceived vehicle injections of the same volume. We observed a significant (P < 0.05) reduction in T-c of similar to 2.8 degrees C after hypoxia (7% insp ired O-2), whereas intraperitoneal injection of 7-NI at 25 mg/kg caused no significant-change in T-c. 7-NI at 30 mg/kg elicited a reduction in T-c and was abandoned in further experiments. When the two treatments were combine d (25 mg/kg of 7-NI and 7% inspired O-2), we observed a significant attenua tion of hypoxia-induced anapyrexia. The data indicate that nNOS plays a rol e in hypoxia-induced anapyrexia.