The antipyretic effect of AVP, α-MSH and ACTH consists in lowering the thrmoregulatory threshold and in shortening the time span of the fever. Thus, neuropeptides influence activity of hypothalamic neurones regulating body temperature. This was confirmed by recent experiments of Moravec (this volume) which indicate that spontaneous activity and thermosensitivity of neurones in hypothalamic slices can be influenced, by AVP. Why neuropeptides of different chemical structure such as AVT, on one hand, and α-MSH and ACTH, on the other hand, induce the same effect on thermoregulation remains to be elucidated.
Apart from thyroid hormones, as the main hormonal regulators of obligatory thermogenesis, and catecholamines, as major hormonal regulators of facultative thermogenesis, production of heat in homeotherms can also be influenced by steroids. Generally, hormones can influence heat production by regulating the activity of various enzymes of oxidative metabolism, by modulating membrane protein carriers and other membrane or nuclear protein factors. Proton carriers in the inner mitochondrial membrane, known as uncoupling proteins, play the key role in heat dissipation to the detriment of the formation of energy-rich phosphates. In this minireview we have focused on the effects of steroids and thyroid hormones on heat production in brown adipose tissues and in skeletal muscles, with particular respect to their effect on uncoupling protein expression. Apart from hormonal steroids, dehydroepiandrosterone, an important precursor in the metabolic pathway leading to hormonal steroids which possess many, mostly beneficial effects on human health, modulates metabolic pathways which may lead to increased heat production. Recent studies demonstrate that 7-oxo-dehydroepiandrosterone, one of its 7-oxygenated metabolites, is even more effective than dehydroepiandrosterone. Recent findings of various actions of these steroids support the view that they may also participate in modulating thermogenic effects.
Using brain slices the effect of prostaglandin E2 (PGE2) on neurones from different locations of the rat hypothalamus was analysed. PGE2 (150 ng), when injected into the perfusion chamber, influences all hypothalamic neurones studied. The pattern of firing rate changes after PGE2 is variable, but the depressive effect predominates - 72 % of neurones decrease their firing rate in long-term experiments. PGE2 also lowers the thermosensitivity of warm sensitive neurones and increases the thermosensitivity of temperature insensitive neurones.
The aim of this study was to ascertain whether repeated local cooling induces the same or different adaptational responses as repeated whole body cooling. Repeated cooling of the legs (immersion into 12 °C water up to the knees for 30 min, 20 times during 4 weeks = local cold adaptation – LCA) attenuated the initial increase in heart rate and blood pressure currently observed in control subjects immersed in cold water up to the knees. After LCA the initial skin temperature decrease tended to be lower, indicating reduced vasoconstriction. Heart rate and systolic blood pressure appeared to be generally lower during rest and during the time course of cooling in LCA humans, when compared to controls. All these changes seem to indicate attenuation of the sympathetic tone. In contrast, the sustained skin temperature in different areas of the body (finger, palm, forearm, thigh, chest) appeared to be generally lower in LCA subjects than in controls (except for temperatures on the forehead). Plasma levels of catecholamines (measured 20 and 40 min after the onset of cooling) were also not influenced by local cold adaptation. Locally cold adapted subjects, when exposed to whole body cold water immersion test, showed no change in the threshold temperature for induction of cold thermogenesis. This indicates that the hypothermic type of cold adaptation, typically occurring after systemic cold adaptation, does not appear after local cold adaptation of the intensity used. It is concluded that in humans the cold adaptation due to repeated local cooling of legs induces different physiological changes than systemic cold adaptation.