{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T13:48:01Z","timestamp":1773150481398,"version":"3.50.1"},"reference-count":36,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1998,9,1]]},"abstract":"<jats:p>Hypercapnia elicits hypothermia in a number of vertebrates, but the mechanisms involved are not well understood. In the present study, we assessed the participation of the nitric oxide (NO) pathway in hypercapnia-induced hypothermia and hyperventilation by means of NO synthase inhibition by using N<jats:sup>\u03c9<\/jats:sup>-nitro-l-arginine (l-NNA). Measurements of ventilation, body temperature, and oxygen consumption were performed in awake unrestrained rats before and afterl-NNA injection (intraperitoneally) and l-NNA injection followed by hypercapnia (5% CO<jats:sub>2<\/jats:sub>). Control animals received saline injections. l-NNA altered the breathing pattern during the control situation but not during hypercapnia. A significant ( P &lt; 0.05) drop in body temperature was measured after bothl-NNA (40 mg\/kg) and 5% inspired CO<jats:sub>2<\/jats:sub>, with a drop in oxygen consumption in the first situation but not in the second. Hypercapnia had no effect onl-NNA-induced hypothermia. The ventilatory response to hypercapnia was not changed byl-NNA, even thoughl-NNA caused a drop in body temperature. The present data indicate that the two responses elicited by hypercapnia, i.e., hyperventilation and hypothermia, do not share NO as a common mediator. 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