Effect of nitric oxide synthase inhibition on hypercapnia-induced hypothermia and hyperventilation

Abstract

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 ω-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% CO2). Control animals received saline injections. l-NNA altered the breathing pattern during the control situation but not during hypercapnia. A significant ( P < 0.05) drop in body temperature was measured after bothl-NNA (40 mg/kg) and 5% inspired CO2, 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. However, thel-arginine-NO pathway participates, although in an unrelated way, in respiratory function and thermoregulation.