Neural mechanism and relationship between cutaneous active vasodilation and sweating and the role of vasodilative peptides and nitric oxide

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On the general skin surface of the humans, cutaneous vasodilation is accompanied by thermal sweating. To elucidate its relationship and neural mechanisms, we studied sweating and skin blood flow responses after administration of nicotine and acetylcholine to the forearm skin. Parallelism of the axone reflex-mediated sweating and skin blood flow indicated that axone reflex sweating is also accompanied by cutaneous vasodilation. Abolishment of sweating but not of cutaneous vasodilation by atropine indicated that vasodilation is mediated by other than muscarinic receptor. In the cat paw sweating model, vasodilation was accompanied by sweating as same as in humans. It is known that acetylcholine, a primary mediator of human sweating, induced vasodilation through NO (nitric oxide) production from the endothelium. Involvement of NO on thermal sweating is strongly expected. Since the vasodilative peptides such as VIP, CGRP and ANP are known to exist around the sweat glands, NO may act on the skin vessels and sweat glands through these peptides. NO-mediated linkage of mechanism of sweating and skin vasodilation is expected to be disclosed in the further studies. The two applied studies using QSART, Quantitative Sudomotor Axone Reflex Test, revealed that thermotolerance of tropical residents is at least in some parts acquired through long-term residence in the tropic environment after the birth and that both of the larger number of forearm sweat glands and the larger sweat output, from a single gland contribute to the men's better thermotolerance compared to the women. In combination of these approaches, studies of the mechanisms on the interrelationship of thermal sweating and active cutaneous vasodilation will be enhanced.