Mogilnicka E, Klimek V, Nowak G, Czyrak A
J Neural Transm. 1985;63(3-4):223-35. doi: 10.1007/BF01252027.
The effects of the alpha-agonist clonidine and the beta-agonist clenbuterol on body temperature of rats kept at high ambient temperature (28 degrees C) were studied. Both drugs induced a dose-dependent significant increase in temperature. The clonidine-induced hyperthermia was blocked by various alpha 2-antagonists, yohimbine, rauwolscine and RX 781094 and the alpha 1-antagonists, prazosin and corynanthine but not by 1-propranolol, spiperone, metergoline. The hyperthermic effect of clonidine was potentiated in rats after a lesion of the central noradrenergic terminals by DSP-4. The clenbuterol-induced hyperthermia was counteracted by 1-propranolol, yohimbine and rauwolscine but not by atenolol, prazosin, spiperone, metergoline. These observations indicate that clonidine- and clenbuterol-induced hyperthermia is mediated by alpha 2-(postsynaptic) and beta-adrenoceptors, respectively. Moreover, in the latter effect alpha 2-adrenoceptors are involved. The simple temperature measurement can thus be used as a preliminary indicator of central alpha 2- or beta-agonistic properties of the screened drug.
研究了α-激动剂可乐定和β-激动剂克伦特罗对处于高环境温度（28摄氏度）的大鼠体温的影响。两种药物均引起剂量依赖性的显著体温升高。可乐定诱导的体温过高被各种α2拮抗剂（育亨宾、萝芙素和RX 781094）以及α1拮抗剂（哌唑嗪和育亨宾碱）阻断，但未被普萘洛尔、螺哌隆、美替拉酮阻断。在经DSP-4损伤中枢去甲肾上腺素能终末的大鼠中，可乐定的升温作用增强。克伦特罗诱导的体温过高被普萘洛尔、育亨宾和萝芙素抵消，但未被阿替洛尔、哌唑嗪、螺哌隆、美替拉酮抵消。这些观察结果表明，可乐定和克伦特罗诱导的体温过高分别由α2（突触后）和β肾上腺素能受体介导。此外，在后一种效应中，α2肾上腺素能受体也参与其中。因此，简单的体温测量可作为所筛选药物中枢α2或β激动特性的初步指标。
