Action of thyroid hormones on the calorigenic effect of adrenaline]

The present investigation was undertaken in order to appraise the interaction between thyroxine and epinephrine in dogs exposed to acute cold. In normal, then successively thyroidectomized, adrenal demedullated and thyroxine restored dogs, epinephrine was infused in basal condition and during acute cold exposure. In thyroidectomized dogs epinephrine lost its calorigenic effects. So it did in thyroidectomized and adrenal demedullated dogs. Conversely, when dogs were restored in thyroxine, epinephrine recovered its calorigenic effect. Evidence for thyroxine-catecholamine interaction can be seen in basal condition as during acute cold. Nevertheless, this interaction is more obvious during shivering thermogenesis.     

TRPA1 agonists--allyl isothiocyanate and cinnamaldehyde--induce adrenaline secretion

Thermosensitive transient receptor potential (TRP) channels, especially TRPV1 and TRPA1, are activated by the pungent compounds present in spices. TRPV1 activation by the intake of capsaicin, the irritant in hot pepper, induces adrenaline secretion and increases energy consumption. TRPV1 is mainly expressed in the sensory neurons and coexpressed with TRPA1 at a high frequency. However, the mechanism underlying adrenaline secretion by TRPA1 agonists such as allyl isothiocyanate (AITC) and cinnamaldehyde (CNA), the pungent ingredients in mustard and cinnamon, is not known. We examined whether AITC and CNA could induce adrenaline secretion in anesthetized rats. An intravenous injection of AITC or CNA (10 mg/kg) increased adrenaline secretion. These responses disappeared completely in capsaicin-treated rats with an impaired sensory nerve function. Moreover, pretreatment with cholinergic blockers (hexamethonium and atropine) attenuated the AITC- or CNA-induced adrenaline secretion. These results suggest that TRPA1 agonists activate the sensory nerves and induce adrenaline secretion via the central nervous system.