Kandasamy S B, Williams B A
Neuropharmacology. 1983 Oct;22(10):1177-81. doi: 10.1016/0028-3908(83)90077-1.
Intracerebroventricular administration of (D-ala2, N-Me-Phe4, Met-(O)5-ol)-enkephalin (FK 33-824) induced dose-related hyperthermia in rabbits and guinea-pigs. Prostaglandins (PG) and norepinephrine (NE) were not involved in the hyperthermia induced by FK 33-824 because a cyclooxygenase inhibitor, indomethacin, and an alpha-adrenoceptor antagonist, phenoxybenzamine, had no antagonistic effects. Likewise, cAMP was not required since a phosphodiesterase inhibitor, theophylline, did not accentuate the hyperthermia due to FK 33-824. It is suggested that mu receptors were involved in the induction of hyperthermia by FK 33-824 in rabbits and guinea-pigs since naloxone attenuated it. These results indicate that FK 33-824-induced hyperthermia is not mediated by PG, NE and cAMP, but rather that mu receptors are involved in the induction of hyperthermia by FK 33-824.
脑室内注射(D-ala2,N-Me-Phe4,Met-(O)5-ol)-脑啡肽(FK 33-824)可在兔和豚鼠中诱导出剂量相关的体温过高。前列腺素(PG)和去甲肾上腺素(NE)不参与FK 33-824诱导的体温过高,因为环氧化酶抑制剂吲哚美辛和α-肾上腺素能受体拮抗剂酚苄明没有拮抗作用。同样,cAMP也不是必需的,因为磷酸二酯酶抑制剂茶碱不会增强FK 33-824引起的体温过高。由于纳洛酮可减弱其作用,提示μ受体参与了兔和豚鼠中FK 33-824诱导的体温过高。这些结果表明,FK 33-824诱导的体温过高不是由PG、NE和cAMP介导的,而是μ受体参与了FK 33-824诱导的体温过高。