Parasympathetic vasodilator nerve fibers do not innervate cutaneous blood vessels. However, stimulation of the sweat glands, which are innervated by sympathetic cholinergic fibers, dilates the skin resistance vessels. Sweat contains an enzyme that lyses a protein (kallidin) in the tissue fluid to produce bradykinin, a polypeptide with potent vasodilator properties. Bradykinin, formed locally, dilates the arterioles and increases blood flow to the skin.
Certain skin vessels, particularly those in the head, neck, shoulders, and upper part of the chest, are regulated by higher centers in the brain. Blushing, in response to embarrassment or anger, and blanching, in response to fear or anxiety, are examples of cerebral inhibition and stimulation, respectively, of the sympathetic nerve fibers to the affected cutaneous regions.
In contrast to AV anastomoses in the skin, the resistance vessels display autoregulation of blood flow and reactive hyperemia. If the arterial inflow to a limb is stopped briefly by inflation of a blood pressure cuff, the skin becomes bright red below the point of vascular occlusion when the cuff is subsequently deflated. The increased cutaneous blood flow (reactive hyperemia) is also manifested by distention of the superficial veins in the affected extremity.
The Role of Temperature in the Regulation of Skin Blood Flow
The primary function of the skin is to maintain a constant internal environment and protect the body from adverse changes. Ambient temperature is one of the most important external variables with which the body must contend. Exposure to cold elicits a generalized cutaneous vasoconstriction that is especially pronounced in the hands and feet. This response is chiefly mediated by the nervous system. Arrest of the circulation to a hand by a pressure cuff plus immersion of that hand in cold water induces vasoconstriction in the skin of the other extremities that are exposed to room temperature. When the circulation to the chilled hand is not occluded, the reflex-generalized vasoconstriction is caused in part by the cooled blood that returns to the general circulation. This returned blood then stimulates the temperature-regulating center in the anterior hypothalamus, which then activates heat preservation centers in the posterior hypothalamus to evoke cutaneous vasoconstriction.
The skin vessels of the cooled hand also respond directly to cold. Moderate cooling or a brief exposure to severe cold (0°C to 15°C) constricts the resistance and capacitance vessels, including the AV anastomoses. Prolonged exposure to severe cold evokes a secondary vasodilator response. Prompt vasoconstriction and severe pain are elicited by immersion of the hand in ice water. However, this response is soon followed by dilation of the skin vessels, with reddening of the immersed part and alleviation of the pain. With continued immersion of the hand, alternating periods of constriction and dilation occur, but the skin temperature rarely drops as much as it did in response to the initial vasoconstriction. Prolonged severe cold, of course, damages tissue. The rosy faces of people exposed to a cold environment are examples of cold-induced vasodilation. However, blood flow through the skin of the face may be greatly reduced despite the flushed appearance. The red color of the slowly flowing blood is mainly caused by reduced O2 uptake by the cold skin and the cold-induced shift of the oxyhemoglobin dissociation curve to the left (see
Direct application of heat to the skin not only dilates the local resistance and capacitance vessels and the AV anastomoses but also reflexively dilates blood vessels in other parts of the body. The local effect is independent of the vascular nerve supply, whereas the reflex vasodilation is a combined response to stimulation of the anterior hypothalamus by the returning warmed blood and stimulation of cutaneous heat receptors in the heated regions of the skin.