Clonidine and a ?-agonists induce hyperthermia in rats at high ambient temperature

Abstract

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.

The thermogenic actions of α2‐adrenoceptor agonists in reserpinized mice are mediated via a central postsynaptic α2‐adrenoceptor mechanism

“…This strongly implies that the OC2-adrenoceptors in question are situated in the central nervous system. A recent report has also suggested that the hyperthermia elicited by clonidine in rats maintained at a high ambient temperature is mediated via central postsynaptic a2-adrenoceptors (Mogilnicka et al, 1985). The results of the present study provide no clue to the mechanisms beyond the level of the central x2-adrenoceptor ultimately responsible for producing an increase in the body temperature of reserpinized mice after the administration of a2-agonists.…”

Adaptive and differential changes on ?- and ?2-adrenoreceptors mediated hyperthermia after chronic treatment with antidepressant drugs in the rat kept at high ambient temperature

“…As we found in our previous paper (Mogilnicka et al, 1985), both a2-and 0~l-adrenoceptors participate in CLON-induced hyperthermia. Since both types of adrenoceptors are involved in the hyperthermic response to CLON, this test does not seem to be specific.…”

“…It seems that the observed alterations result from changes in a2-adrenoceptors postsynaptic since, as was found in previous papers, the a2-adrenoceptors that mediate CLON-induced sedation or hyperthermia are located postsynaptically (Mogilnicka et al, 1985;Spyraki and Fibiger, 1982).…”

“…In our recent paper (Mogilnicka et al, 1985) we showed that the fl-agonist clenbuterol (CLEN) or the 0~2-agonist clonidine (CLON) given to rats at high ambient temperature (AT), induced hyperthermia mediated by fl-adrenoceptors or ~zz-adrenoceptors, respectively. These tests may be useful for assessing the fl-or cq-agonistic properties of drugs.…”

Simultaneous telemetric monitoring of tail-skin and core body temperature in a rat model of thermoregulatory dysfunction

“…These studies required separate surgical implantations using different groups of animals to record changes in TST and CBT measurements. The compounds, clonidine (alpha 2 adrenergic agonist) (Mogilnicka et al, 1985), MDL-100907 (MDL, 5-HT 2a antagonist) (Sipe et al, 2004) and 17␣-ethinyl estradiol (EE, estrogen receptor agonist) (Sipe et al, 2004) have been previously reported to affect temperature in rats but the temporal relationship between TST and CBT has not been reported. Therefore, these test compounds were used to compare the sensitivity and reproducibility of the two types of temperature probes.…”