The Normal Structure and Function of the Cutaneous Vascular System

During exposure to cold, our bodies strive to maintain normal core temperature by restricting heat loss, which is mediated by reducing blood flow to the skin (cutaneous vasoconstriction) and by increasing heat production (shivering and non-shivering thermogenesis). Blood vessels in the skin have specialized structural and functional features that enable them to contribute to thermoregulation. Arteriovenous anastomoses (AVAs) are direct connections between arterioles and venules that bypass nutritional capillaries and allow markedly increased blood flow to the skin. When there is a need for heat conservation, AVAs remain constricted, whereas during heat elimination, they are fully dilated. Cold exposure increases the activity of the sympathetic adrenergic nervous system, which is responsible for initiating cutaneous vasoconstriction and for activating non-shivering thermogenesis in skeletal muscle and brown adipose tissue. The increase in sympathetic outflow is mediated by the activation of thermosensitive neurons and is likely mediated by the stimulation of cold-sensitive ion channels such as TRPM8. Local cooling of the extremities further amplifies the vasoconstrictor response to sympathetic nerve activity. The sympathetic activity and local cooling-induced augmentation of that constriction acts selectively to restrict blood flow through AVAs, preserving nutritional blood flow through skin capillaries. A key component of cold-induced cutaneous vasoconstriction is the activation of smooth muscle α2-ARs. These receptors are activated preferentially by norepinephrine released from sympathetic nerves in cutaneous blood vessels (including AVAs), and their reactivity is dramatically increased by local cooling. Local cooling also stimulates cutaneous dilatation by increasing endothelium-derived hyperpolarization. This response likely acts to restrain cold-induced vasoconstriction and facilitate restoration of normal blood flow during rewarming. The influence of estrogen makes the female cutaneous vascular system especially sensitive to sympathetic and cold-induced constriction.