[Role of sympatho-adrenomedullar system in adaptation to cold]

It was persuasively shown that norepinephrine released from sympathetic nervous endings plays an important role in the adaptation to cold and epinephrine secreted by adrenal medulla. After acclimatization calorigenic effect of norepinephrine is enhanced. Catecholamines stimulate nonshivering thermogenesis in brown adipose tissue and apparently in white adipose tissue and in skeletal muscles. Adrenergic enhancement of tolerance to cold is depended upon an increase in UCP expression in tissues. In realization of calorigenic effect of catecholamines during long-term cold exposures it is participated following signaling pathway: catecholamines --> β-adrenergic receptors (AR) --> adenylyl cyclase --> cAMP --> protein kinase A --> p38 kinase --> transcription factors --> enhancement of UCP expression. At acute cold exposure it was realized catecholamines --> β-AR --> adenylyl cyclase --> cAMP --> protein kinase A --> hormone sensitive lipase --> free fatty acids --> UCP --> uncoupling oxidative phosphorylation. Calorigenic effect of α1--AR stimulation is realized by following mechanism: norepinephrine --> α1-AR --> phospolipase C --> inositol 1,4,5-triphosphate -->[Ca2+]i --> enhancement of calorigenic effect of catecholamines.