Vago-sympathoadrenal reflex in thermogenesis induced by osmotic stimulation of the intestines in the rat.
Duodenal infusion of hypertonic solutions elicits osmolality-dependent thermogenesis in urethane-anaesthetized rats. Here we investigated the involvement of the autonomic nervous system, adrenal medulla and brain in the mechanism of this thermogenesis. Bilateral subdiaphragmatic vagotomy greatly attenuated the first hour, but not the later phase, of the thermogenesis induced by 3.6 % NaCl (10 ml kg(-1)). Neither atropine pretreatment (10 mg kg(-1), I.P.) nor capsaicin desensitization had any effect on the osmotically induced thermogenesis, suggesting the involvement of non-nociceptive vagal afferents. Bilateral splanchnic denervation caudal to the suprarenal ganglia also had no effect, suggesting a lack of involvement of spinal afferents and sympathetic efferents to the major upper abdominal organs. Adrenal demedullation greatly attenuated the initial phase, but not the later phase, of thermogenesis. Pretreatment with the beta-blocker propranolol (20 mg kg(-1), I.P.) attenuated the thermogenesis throughout the 3 h observation period. The plasma adrenaline concentration increased significantly 20 min after osmotic stimulation but returned to the basal level after 60 min. The plasma noradrenaline concentration increased 20 min after osmotic stimulation and remained significantly elevated for 120 min. Therefore, adrenaline largely mediated the initial phase of thermogenesis, and noradrenaline was involved in the entire thermogenic response. Moreover, neither decerebration nor pretreatment with the antipyretic indomethacin (10 mg kg(-1), S.C.) had any effect. Accordingly, this thermogenesis did not require the forebrain and was different from that associated with fever. These results show the critical involvement of the vagal afferents, hindbrain and sympathoadrenal system in the thermogenesis induced by osmotic stimulation of the intestines.
Osaka
Toshimasa
T
National Institute of Health and Nutrition, Shinjuku 162-8636, Japan. osaka@nih.go.jp
Kobayashi
Akiko
A
Inoue
Shuji
S
D000311:Adrenal Glands / Q000502:physiology*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D002395:Catecholamines / Q000502:physiology; D003655:Decerebrate State / Q000503:physiopathology; D004032:Diet; D004734:Energy Metabolism / Q000502:physiology; D005268:Femoral Vein / Q000502:physiology; D007031:Hypothalamus / Q000502:physiology; D007213:Indomethacin / Q000494:pharmacology; D007422:Intestines / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009475:Neurons, Afferent / Q000502:physiology; D011169:Portal Vein / Q000502:physiology; D016548:Prosencephalon / Q000502:physiology; D011453:Prostaglandins / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D012018:Reflex / Q000502:physiology*; D012462:Saline Solution, Hypertonic / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000502:physiology*; D022722:Thermogenesis / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D002395:Catecholamines; D011453:Prostaglandins; D011943:Receptors, Adrenergic, beta; D012462:Saline Solution, Hypertonic; D007213:Indomethacin