Heat loss and heat production induced by capsaicin.

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Subcutaneous administration of capsaicin (5 mg/kg) immediately increased the temperature of the tail skin for 2 h in urethan-anesthetized rats, suggesting an increase in heat loss. Oxygen consumption, an index of heat production, also immediately increased after the capsaicin injection, and this increase lasted for more than 10 h. Colonic temperature decreased within 1 h after the injection, and this decrease was followed by a long-lasting hyperthermic period. Adrenal demedullation largely attenuated the capsaicin-induced heat production, and sympathetic denervation of the interscapular brown adipose tissue (IBAT) partly did so. However, capsaicin-induced heat loss was normal in these rats. In rats with cutaneous vasodilatation maximized, capsaicin did not further increase heat loss but normally induced heat production. Thus, capsaicin simultaneously activates independent networks for heat loss and heat production.Next, we examined the function of capsaicin-sensitive sensory fibers that innervate IBAT.Warming of the IBAT to 40-44ﾟC attenuated the subsequent noradrenaline-induced thermogenesis (NIT) of the IBAT.In this range of warming, higher IBAT temperatures resulted in more attenuation. Administration of 5.2 nmol CGRP but not substance P or vehicle saline mimicked the effect of thermal stimulation of IBAT.Administration of capsacin (1 mg/kg, s.c.) also attenuated the NIT.Denervation of the IBAT or pretreatment with capsazepine, a capsaicin receptor antagonist, blocked the effect of capsaicin. We propose that temperature- and capsaicin-sensitive nerve fibers release CGRP to attenuate the NIT of brown adipocytes.