RT Journal Article
SR Electronic
T1 Role of the Nitric-Oxide Synthase Isoforms during Morphine-Induced Hyperthermia in Rats
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 219
OP 222
DO 10.1124/jpet.103.053181
VO 307
IS 1
A1 Khalid Benamar
A1 Menachem Z. Yondorf
A1 David Kon
A1 Ellen B. Geller
A1 Martin W. Adler
YR 2003
UL http://jpet.aspetjournals.org/content/307/1/219.abstract
AB Recently, we demonstrated that the diffusible messenger molecule nitric oxide (NO) is involved in the hyperthermic response induced by morphine by using a nonselective nitric-oxide synthase inhibitor, N-nitro-l-arginine methyl ester. The present work extended these studies to include 7-nitroindazole (7-NI), an inhibitor specific for neuronal nitric-oxide synthase (nNOS), N(5)-(-iminoethyl)-l-ornithine (l-NIO), an inhibitor of endothelial NOS (eNOS), and aminoguanidine (AG), a potent inhibitor of inducible NOS (iNOS). A biotelemetry system was used in this study to measure the body temperature (Tb). A dose of 7-NI (5 or 10 mg/kg), which did not affect Tb by itself, blocked the hyperthermia induced by morphine in a dose-dependent manner (15 mg/kg i.p.). However, pretreatment with l-NIO (10–20 mg/kg) or with AG (50 mg/kg) failed to alter the hyperthermia induced by morphine. l-NIO (10–20 mg/kg) or AG (50 mg/kg) had no effect on Tb. These results suggest the involvement of nNOS in morphine-induced hyperthermia. The American Society for Pharmacology and Experimental Therapeutics