Nitric oxide mediates noradrenaline-induced hypothermic responses and opposes prostaglandin E2-induced fever in the rostromedial preoptic area

Noradrenaline (NA) microinjected into the rostromedial preoptic area (POA) elicits heat loss responses and opposes prostaglandin E2-induced fever. Here, I tested the hypothesis that local synthesis and release of nitric oxide (NO) mediates the NA-induced effects. The unilateral microinjection of the NO donor sodium nitroprusside (SNP, 8.4 nmol), but not that of saline solution, into the NA-sensitive site elicited an increase in tail skin temperature and decreases in the whole-body O2 consumption rate, heart rate, and colonic temperature simultaneously in urethane–chloralose-anesthetized rats. Pretreatment with SNP greatly attenuated the thermogenic, tachycardic, and hyperthermic effects of prostaglandin E2 (140 fmol) microinjected into the same site. Furthermore, the NA-induced hypothermic responses were largely blocked by a prior microinjection of an NO synthase inhibitor NG-monomethyl-l-arginine (l-NMMA, 5 nmol), but not by that of its inactive enantiomer, NG-monomethyl-d-arginine (d-NMMA, 5 nmol), at the same site. These results suggest that the hypothermic and antipyretic effects of NA are mediated by NO in the rostromedial POA.