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Sympathetic Control of Sweating and Cutaneous Active Vasodilatation

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Thermotherapy for Neoplasia, Inflammation, and Pain

Summary

Eccrine sweat glands are innervated by postganglionic cholinergic fibers. Activities of these fibers, which can be percutaneously recorded as multiunit burst activities using a microelectrode technique, are controlled by central mechanisms. There are two distinctive central mechanisms for sweating. The central mechanism that governs the sweat glands in the general body surface, except the palm and the sole, involves the detection of local temperature and the integration of thermal and nonthermal signals. The preoptic and anterior hypothalamus is an important region for these functions. The thermal signals from various sites of the body (including the CNS and the skin) are integrated at thermosensitive neurons in these areas, and sudomotor signals are generated. Nonthermal signals also converge to these neurons to modify the thermosensitivity of the central mechanism and, thus, the sudomotor outflow. In this way, they contribute to the preservation of homeostasis in situations of competition between thermal and nonthermal drives. The central mechanism that governs the skin of the palm and the sole probably involves several CNS structures including the reticular formation, limbic system, and neocortex. Mental stimuli not only elicit responses in sudomotor nerve activity destined for the palm and the sole, but also influence the central mechanism for generalized sweating to alter sudomotor outflow to the general body surface. Several neuropeptides are found in the nerve terminals around the sweat gland. These peptides may have a role in increasing local blood flow. The hypothesis has been proposed that sudomotor efferents also mediate active cutaneous vasodilatation.

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Sugenoya, J., Matsumoto, T., Nishiyama, T., Sakamoto, Y. (2001). Sympathetic Control of Sweating and Cutaneous Active Vasodilatation. In: Kosaka, M., Sugahara, T., Schmidt, K.L., Simon, E. (eds) Thermotherapy for Neoplasia, Inflammation, and Pain. Springer, Tokyo. https://doi.org/10.1007/978-4-431-67035-3_20

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