Hypoxic activation of arterial chemoreceptors inhibits sympathetic outflow to brown adipose tissue in rats

• Published in: The Journal of physiology Vol. 566; no. 2; pp. 559 - 573
• Main Authors: Madden, C. J., Morrison, S. F.
• Format: Journal Article
• Language: English
• Published: 9600 Garsington Road , Oxford , OX4 2DQ , UK The Physiological Society 15-07-2005; Blackwell Science Ltd; Blackwell Science Inc
• Subjects: Adipose Tissue, Brown - innervation; Adipose Tissue, Brown - physiology; Animals; Arteries - physiology; Bicuculline - pharmacology; Body Temperature - drug effects; Body Temperature - physiology; Carotid Body - metabolism; Chemoreceptor Cells - physiology; Denervation; Dinoprostone - pharmacology; Enzyme Inhibitors - pharmacology; GABA Agonists - pharmacology; GABA Antagonists - pharmacology; Hemodynamics - drug effects; Hemodynamics - physiology; Hypoxia - metabolism; Integrative Physiology; Male; Microinjections; Muscimol - pharmacology; Preoptic Area - physiology; Rats; Rats, Sprague-Dawley; Respiratory Mechanics - drug effects; Respiratory Mechanics - physiology; Sodium Cyanide - pharmacology; Sympathetic Nervous System - physiology
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.2005.086322

In urethane–chloralose anaesthetized, neuromuscularly blocked, artificially ventilated rats, we demonstrated that activation
of carotid chemoreceptors inhibits the elevated levels of brown adipose tissue (BAT) sympathetic nerve activity (SNA) evoked
by hypothermia, by microinjection of prostaglandin E 2 into the medial preoptic area or by disinhibition of neurones in the raphe pallidus area (RPa). Peripheral chemoreceptor
stimulation with systemic administration of NaCN (50 μg in 0.1 ml) or with hypoxic ventilation (8% O 2 –92% N 2 , 30 s) completely inhibited BAT SNA. Arterial chemoreceptor-evoked inhibition of BAT SNA was eliminated by prior bilateral
transections of the carotid sinus nerves or by prior inhibition of neurones within the commissural nucleus tractus solitarii
(commNTS) with glycine (40 nmol/80 nl) or with the GABA A receptor agonist muscimol (160 pmol/80 nl; 77 ± 10% attenuation), or by prior blockade of ionotropic excitatory amino acid
receptors in the commNTS with kynurenate (8 nmol/80 nl; 82 ± 10% attenuation). Furthermore, activation of commNTS neurones
following local microinjection of bicuculline (30 pmol/60 nl) completely inhibited the elevated level of BAT SNA resulting
from disinhibition of neurones in the RPa. These results demonstrate that hypoxic stimulation of arterial chemoreceptor afferents
leads to an inhibition of BAT SNA and BAT thermogenesis through an EAA-mediated activation of second-order, arterial chemoreceptor
neurones in the commNTS. Peripheral chemoreceptor-evoked inhibition of BAT SNA could directly contribute to (or be permissive
for) the hypoxia-evoked reductions in body temperature and oxygen consumption that serve as an adaptive response to decreased
oxygen availability.