Thermoregulation: The Normal Structure and Function of the Cutaneous Vascular System

During exposure to cold, our bodies attempt 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 (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 need for heat conservation AVAs remain constricted, whereas during heat elimination they are fully dilated. Cold exposure increases the activity of the sympathetic nervous system, which is responsible for initiating cutaneous vasoconstriction. Local cooling of the extremities further amplifies the vasoconstrictor response to sympathetic nerve activity. Sympathetic vasoconstriction and local cold-induced amplification act selectively to restrict blood flow through AVAs, preserving nutritional blood flow through skin capillaries. Multiple mechanisms can contribute to sympathetic and local cold-induced amplification of vasoconstriction. However, a key component is activation of smooth muscle α2-ARs. The female cutaneous vascular system is especially sensitive to thermal challenges (warm and cold).