Vascular tone, also known as vasoconstriction, is the result of contractions of the tunica media. Either these contractions are triggered by an increase in sympathetic tone or they are hormonally controlled. Pathological vasoconstrictions are symptomatic, for example, in atherosclerotic plaques.
What is vascular constriction?
Vascular constriction is defined by physicians as a narrowing of the blood vessels caused by contraction of the tunica media (vascular muscles). The blood vessels in the human body are equipped with the so-called vascular musculature. This smooth tunica media is capable of toning the blood and lymph channels by contraction. It responds to hormonal and neuronal stimuli. Vascular tone is understood by physicians to be a constriction of the blood vessels caused by contraction of the tunica media. Blood flow is reduced by contraction of the vascular musculature, as this decreases the lumen of the vessels. This muscular-induced and blood pressure-regulating constriction of the vessels is also called vasoconstriction. Relaxation of the tunica media is called vasodilation and is the opposite of vasoconstriction. The blood vessels expand during vasodilation, increasing their lumen. Blood flow is thus increased. Vasodilatation and vasoconstriction can be deliberately induced by various substances. If the tunica media is to be stimulated to contract, this is done, for example, by the administration of so-called vasoconstrictors.
Function and task
Physiologic vasoconstriction is triggered by neuronal stimuli from the sympathetic nervous system and by hormonal stimuli. The reduction in vascular cross-section also decreases blood flow behind the respective gating of the blood vessels. The contraction of the smooth tunica media required for this is controlled by visceromotor nerve fibers in the autonomic nervous system and is triggered either by an increase in sympathetic tone or by messenger substances such as AVP, epinephrine, and thromboxane. Vascular tone mainly affects smaller arteries and plays a role in endogenous processes such as sympathetic-mediated thermoregulation. Thermoregulatory processes are controlled by the hypothalamus and depend on the tone of the sympathetic nervous system. High toni indicate heat loss to the hypothalamus. However, the body temperature of a warm-blooded animal must be kept relatively constant in the warm range to maintain an ideal environment for properties such as nerve conduction. The hypothalamus therefore initiates a counter-regulatory response when heat loss occurs. This includes, for example, vasoconstriction. In the peripheral blood vessels, a high tone of the sympathetic nervous system thus leads to a-adrenergic vasoconstriction, which throttles blood flow in the extremities. On the body surface, the higher the blood flow, the more heat loss occurs. Thus, with thermoregulatory restriction of blood flow, heat is conserved when temperatures are cold or heat loss is otherwise imminent. However, vasoconstriction can also be initiated by hormones. Blood vessels are equipped with certain receptors, such as the so-called α-receptors for noradrenaline. Hormones such as angiotensin, serotonin or thromboxane A2, endothelin and norepinephrine bind to these receptors. In a state of shock, for example, certain hormones can ensure that not too much blood escapes from open wounds. Stress hormones and shock hormones such as adrenaline, for example, mediate smooth muscle contraction in organs with a1 adrenoreceptors. Physiologically, open wounds bleed profusely initially to flush contaminants from the tissues. However, the release of vasoconstrictor hormones causes the wounds to bleed hardly at all after some time in order to prevent greater blood loss. Adrenaline is therefore used in medicine, for example, for local vasoconstriction to stop bleeding.
Diseases and ailments
In reversible cerebral vasoconstriction syndrome, the mechanism of vasoconstriction is affected by pathological phenomena. The condition is also called Call-Fleming syndrome and triggers constriction of the cerebral vessels, which can cause headaches and promote strokes. Epileptic seizures may also occur as part of the disease. Patients of all ages are affected.Vascular position also plays a role in phenomena such as the Bayliss effect, which describes the contraction response of blood vessels in regulating local blood circulation to maintain constant organ and tissue perfusion. The Bayliss effect primarily affects the kidneys, gastrointestinal tract, and brain. When blood pressure increases, the wall dilation of the arteries changes in the aforementioned organs, although this is automatically compensated for by the contraction of the tunica media. Only when the intravascular pressure decreases does the vascular smooth muscle open up again. In this way, a constant organ perfusion is maintained even during fluctuations in blood pressure. This type of circulatory regulation is independent of autonomic innervation. Medically, this effect plays a role especially for nerve injuries. If such injuries are present, then the Bayliss effect is maintained. Thus, if the effect can no longer be observed, more than just a nerve injury is present. Vascular constriction is also a symptom of atherosclerotic plaques and, in the context of atherosclerosis, is triggered by a malfunction of the endothelium, whose substances prevent the accumulation of blood cells in the course of the disease. In contrast, pathological vascularization of the renal vessels is present in hepatorenal syndrome, which can cause oliguric renal failure in patients with liver disease. Vascularization also plays a role in hypoxic pulmonary vasoconstriction in the context of the ventilation-perfusion relationship of the lungs. In all diseases with alveolar hypoxia, symptoms related to hypoxic pulmonary vasoconstriction occur, for example, in pneumonia or chronic obstructive pulmonary disease.
