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INFLAMMATION, CYTOKINES, AND TEMPERATURE REGULATION

Preoptic ₁- and ₂-noradrenergic agonists induce, respectively, PGE₂-independent and PGE₂-dependent hyperthermic responses in guinea pigs

Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163

Submitted 25 August 2003 ; accepted in final form 8 February 2004

We have shown previously that norepinephrine (NE) microdialyzed into the preoptic area (POA) of conscious guinea pigs stimulates local PGE₂ release. To identify the cyclooxygenase (COX) isozyme that catalyzes the production of this PGE₂ and the adrenoceptor (AR) subtype that mediates this effect, we microdialyzed for 6 h NE, cirazoline (₁-AR agonist), and clonidine (₂-AR agonist) into the POA of conscious guinea pigs pretreated intrapreoptically (intra-POA) with SC-560 (COX-1 inhibitor) or nimesulide or MK-0663 (COX-2 inhibitors) and measured the animals' core temperature (T_c) and intra-POA PGE₂ responses. Cirazoline induced T_c rises promptly after the onset of its dialysis without altering PGE₂ levels. NE and clonidine caused early falls followed by late rises of T_c; intra-POA PGE₂ levels were closely correlated with this thermal course. COX-1 inhibition attenuated the clonidine-induced T_c and PGE₂ falls but not the NE-elicited hyperthermia, but COX-2 inhibition suppressed both the clonidine- and NE-induced T_c and PGE₂ rises. Coinfused cirazoline and clonidine reproduced the late T_c rise of clonidine but not its early fall and also not the early rise produced by cirazoline; on the other hand, the PGE₂ responses were similar to those to NE. Prazosin (₁-AR antagonist) and yohimbine (₂-AR antagonist) blocked the effects of their respective agonists. These results indicate that ₁- and ₂-AR agonists microdialyzed into the POA of conscious guinea pigs evoke distinct T_c responses: ₁-AR activation produces quick, PGE₂-independent T_c rises, and ₂-AR stimulation causes an early T_c fall and a late, COX-2/PGE₂-dependent T_c rise.

thermoregulation; cyclooxygenase inhibitors; prostaglandin E₂; noradrenergic agonists and antagonists; care temperature; norepinephrine

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