Vasodilation is a widening of the vessels by relaxation of the vascular smooth muscle. This smooth muscle is controlled by the two antagonists, sympathetic and parasympathetic, in the autonomic nervous system. In anaphylactic (allergic) shock, vasodilation of life-threatening proportions is present.
What is vasodilation?
Vasodilation is a widening of the vessels due to relaxation of the vascular muscles. The autonomic nervous system controls a variety of vital body processes. The heartbeat, digestion, metabolism or blood pressure cannot be influenced voluntarily, but are all controlled by higher-level brain centers and hormones. Nerve impulses quickly adapt organ functions to changing circumstances. Especially the nerve pathways of the antagonists sympathetic and parasympathetic nervous system determined the activities of the autonomic nervous system. They lead from the central nervous system to the individual organs. All involuntarily controlled nerve fibers are called visceromotor nerve fibers and are subject to either parasympathetic or sympathetic control. The vasculature contains visceromotor fibers of both sympathetic and parasympathetic control. Vasodilation is the involuntary relaxation of vascular smooth muscle caused indirectly by the parasympathetic nervous system. Relaxation of the musculature dilates the vessels, thus increasing blood flow. The opposite of this relaxation process is vasoconstriction, which is performed by the sympathetic nervous system and causes the vascular muscles to tighten. The lumen of the vessels is thus narrowed and blood flow decreases.
Function and purpose
Vasodilation and vasoconstriction are vital processes of the autonomic nervous system. They adjust blood flow to changing circumstances and thus are required to maintain circulation. Blood flow that is too sudden could overload the heart. Too little blood flow could cause tissue or internal organs to perish because of an inadequate supply of oxygen. The tuning of blood flow to a given situation does not have to be consciously decided, but occurs automatically. This automaticity is especially useful for responding as quickly as possible to changing situations. The active control of vascular smooth muscle lies mainly with the sympathetic nervous system. It causes the muscles to contract permanently. The parasympathetic nervous system is responsible for vasodilation. Since it acts as an antagonist of the sympathetic nervous system, it has an inhibitory effect on the influence of the sympathetic nervous system. This inhibition can weaken or invalidate the contraction command of the sympathetic nervous system. The vascular muscles relax and the blood vessels increase their lumen. As a result, blood flow increases. Vasodilation can be brought about both actively and passively. The active procedure is relaxation of the vascular muscles. Passive vasodilation, on the other hand, occurs when blood volume increases. In active vasodilation, the interaction of nerves and muscles is referred to as vasomotor activity. Vasodilation is also controlled by local mediators in addition to visceromotor fibers. Bradykinin, acetylcholine, or endothelin appear as such mediators, stimulating endothelial receptors. As such, the B2, the M3, and the ET-B receptors are grouped together. These receptors respond to stimulation with the formation of nitric oxide and prostacyclin. The parasympathetic nervous system perceives the increased nitric oxide concentration as a request to inhibit the sympathetic nervous system. Thus, it exerts an influence on the sympathetic nervous system, allowing the vessels to relax. The role of nitric oxide is evident in flow-mediated vasodilation, which is triggered by flow-induced shear forces. The prerequisite for flow-mediated vasodilation is the work of the endothelium. Activation of endothelial potassium channels allows potassium to flow out, evoking hyperpolarization. Calcium influx activates endothelial nitric oxide synthases.
Diseases and disorders
One of the most common complaints associated with vasodilation and vasoconstriction is migraine headache. Insufficient vasodilation of cerebral vessels triggers this type of headache. Vasoactive substances or relaxation training such as autogenic training can induce vasodilation, which can relieve the headache.Damage to the endothelium can also be associated with vasodilation disorders. For example, if the endothelium no longer senses shear forces, its potassium channels do not open and nitric oxide synthases are not activated in sufficient quantity. Flow-mediated vasodilation is therefore frequently determined clinically to draw conclusions about endothelial activity. Vasodilatation-related symptoms and complications may also occur in the context of allergic reactions. In the case of vasodilation, this can involve the release of histamine. This substance not only dilates the blood vessels, but also reddens the skin and, in extreme cases, can trigger anaphylactic shock. In the course of an anaphylactic shock, circulatory collapse and organ failure can occur. The immune system shows such a reaction, for example, to chemical substances. The increased release of mediators constricts the bronchial tubes and causes gastrointestinal symptoms. This systemic reaction of the entire organism is potentially life-threatening. It causes blood pressure to drop sharply because of vasodilatation. Fluid leaks from the vessels into the surrounding tissues. The pulse drops and unconsciousness sets in. Initial symptoms are relatively nonspecific and range from vomiting to visual disturbances and dry mouth to shortness of breath and circulatory problems. Anaphylactic shock can ultimately cause circulatory and respiratory arrest. This life-threatening situation can only be reversed by rapid resuscitation. Adrenaline and similar substances can relieve the acute symptoms under certain circumstances. Glucocorticoids and antihistamines or H2 receptor antagonists may also improve the patient’s condition.
