The autonomic nervous system controls a variety of vital body processes. The heartbeat, digestion, metabolism or blood pressure can not be deliberately influenced, but are all controlled by superordinate brain centers and hormones.
Nerve impulses quickly adapt the organ functions to changed circumstances. Specifically, the neural pathways of the antagonist sympathetic and parasympathetic 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 vascular system contains both visceromotor fibers sympathetic, as well as parasympathetic control.
Vasodilation is the involuntary relaxation of vascular smooth muscle caused indirectly by the parasympathetic nervous system. The relaxation of the muscles expands the vessels and thus increases the blood flow. The opposite of this relaxation process is the vasoconstriction, which is performed by the sympathetic and which makes the vascular musculature to tighten. The lumen of the vessels is thus narrowed and the blood flow lowers.
Vasodilatation and vasoconstriction are vital processes of the autonomic nervous system. They adapt the blood flow to changed circumstances and are thus necessary for the maintenance of the circulation. Too sudden blood flow could overload the heart. Too little blood flow could kill tissue or internal organs due to a shortage of oxygen.
The coordination of the blood flow to a given situation does not have to be decided consciously, but takes place automatically. This automatic is especially helpful for the quickest possible reaction to changed situations. The active control of vascular smooth muscle is mainly in the sympathetic. It causes the muscles to contract permanently. The parasympathetic nervous system is responsible for vasodilation. Since he appears as an opponent of the sympathetic, he acts inhibiting the influence of the sympathetic. This inhibition may attenuate or invalidate the contraction command of the sympathetic. The vascular muscles relax and the blood vessels increase their lumen. This increases the blood flow.
Vasodilatation can be induced both actively and passively. An active procedure is the relaxation of the vascular musculature. Passive vasodilation, on the other hand, occurs with an increase in blood volume. In active vasodilation, the interaction of nerves and muscles is called vasomotor function.
Vasodilation is also controlled by local mediators in addition to visceromotor fibers. As such mediators, bradykinin, acetylcholine or endothelin appear to stimulate the endothelial receptors. As such, the B2, M3 and 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 an invitation to inhibit the sympathetic nervous system. Thus, it influences the sympathetic and lets the vessels relax.
The role of nitric oxide is shown in flow-mediated vasodilation, which is triggered by flow-induced shear forces. The prerequisite for flow-mediated vasodilation is the work of the endothelium. The activation of endothelial potassium channels causes potassium to escape, causing hyperpolarization. Calcium enters and activates endothelial nitric oxide synthases.
One of the most common ailments related to vasodilation and vasoconstriction is migraine headache. Inadequate vasodilation of the cerebral vessels triggers this type of headache. Vasoactive substances or relaxation training such as autogenic training can cause vasodilatation, which can relieve headache.
Damage to the endothelium may 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. The flow-mediated vasodilation is therefore clinically often determined to draw conclusions about the activity of the endothelium.
Vascular ailments and complications may also occur as part of allergic reactions. In case of vasodilation, the release of histamine can be carried out. This substance not only dilates the blood vessels, but also reddens the skin and can cause anaphylactic shock in extreme cases. Anaphylactic shock can cause circulatory collapse and organ failure. Such a reaction shows the immune system, for example, on chemical substances. The increased released mediators make the bronchi tight and cause gastrointestinal symptoms.
This systemic response of the entire organism is potentially life threatening. It causes the blood pressure to drop sharply due to the dilation of the vessels. Fluid escapes from the vessels into the surrounding tissue. The pulse drops and unconsciousness occurs. The initial symptoms are relatively nonspecific, ranging from vomiting, blurred vision and dry mouth to respiratory distress and circulatory distress.
Anaphylactic shock can ultimately trigger a circulatory and respiratory arrest. This life-threatening situation can only be remedied by rapid resuscitation. Epinephrine and similar substances may alleviate the acute symptoms. Glucocorticoids and antihistamines or H2 receptor antagonists can also improve the condition of the patient.