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Lefty-Loosey, Righty-Tighty: the Autonomic Nervous System, Blood Vessels and POTS


Pistol

By Susanne Rimm

Many symptoms experienced by people living with POTS and other dysautonomias are related to a miscommunication within the Autonomic Nervous System) (ANS) between the sympathetic and the parasympathetic systems. The ANS controls the pressure inside our blood vessels.  This complicated process involves many aspects of anatomy ( heart and vasculature ), hormones, chemicals, and nerves. 

Efficient circulation is necessary to provide the body systems with adequate oxygen and nutrition to perform their specific tasks. Some organs or parts of the body need a constant rate of circulation ( i.e., the brain ), and some need more at certain times ( i.e., the digestive tract ). Maintaining and directing blood flow within the body is dependent on the harmonious communication between the sympathetic and parasympathetic nervous systems. These systems influence blood flow by widening the blood vessels (vasodilation) or tightening the vessels (vasoconstriction).   Vasodilation lowers the pressure within the vessels vs. vasoconstriction which raises the pressure. These systems respond differently to various triggers within the body ( endogenous ) and from outside of the body ( exogenous ). 

What are blood vessels?

Blood vessels are precisely that – vessels that transport blood. Anatomically they are tubular structures with an inner lining (endothelium), which is surrounded by connective tissue. They contain smooth muscle cells that respond to small nerve fibers directly connected to the ANS. Arteries carry oxygenated blood from the heart through the body, and veins return the blood through the lungs to the heart. 

vasodilation.jpg.7cc4d334b2cc27c2fc65421ea30a1a9b.jpgVasodilation

Widening of blood vessels increases blood flow, lowers blood pressure, and occurs when the smooth muscle cells within the walls relax. This can occur in response to endogenous factors such as hormones, chemicals, or nerve impulses. An increase in carbon dioxide, potassium ions, hydrogen ions, and adenosine can all lead to vasodilation. Another cause is the release of the hormone epinephrine caused by the activation of beta-2 receptors in the muscles of the blood vessels. Other causes for vasodilation are the release of nitrous oxide ( a substance released by certain nerves during inflammation ) as well as the release of histamine.  (1,2)

Exogenous factors that can cause vasodilation are heat, certain foods, or beverages (e.g. alcohol ) or light and noises from the environment. Pharmaceuticals can also cause vasodilation and can be used to treat certain conditions like angina or hypertension.  Vasodilation can lead to hot, flushed skin by drawing circulation to the periphery and away from the core. Other symptoms include sweating, tachycardia, nausea, dizziness, vision and hearing changes, headaches, and more. (1,2)

Vasoconstriction 

Narrowing of blood vessels occurs when the smooth muscles of the vessel walls constrict, resulting in restricted blood flow.  This increase in vascular resistance raises systemic blood pressure and causes a localized reduction in blood flow. The general mechanism leading to vasoconstriction is an increased concentration of calcium ions in the smooth muscle cells.  This concentration occurs because of an increase in epinephrine or activation of the sympathetic nervous system through the release of norepinephrine. These neurotransmitters interact with adrenergic receptors. 

Again, vasoconstriction can be caused by endogenous and exogenous factors. Examples for exogenous causes are exposure to severe cold temperatures, which cause the cutaneous vessels to constrict in an attempt to reroute the circulating blood to the core. This constriction is what causes the skin to become pale in cold weather as less blood reaches the surface.  Medications such as antihistamines, amphetamines, or stimulants are vasoconstrictors. They can be used to increase blood pressure or reduce local blood flow.     

The most crucial endogenous trigger for vasoconstriction is the normal attempt of the ANS to correct the sudden drop in blood pressure that occurs when standing to avert orthostatic hypotension.  A critical trigger for vasoconstriction is the narrowing of blood vessels necessary during sudden hemorrhage. As the body attempts to stop or limit blood loss, circulation is diverted towards vital organs and away from the source of the bleeding.  The more common symptoms of vasoconstriction are tremors, cold extremities, paleness or bluish color skin, tachycardia, palpitations, chest pains, and more. (3)                                                                              

Autonomic Tone

Autonomic Tone is the balance of sympathetic and parasympathetic activity. It is regulated by the hypothalamus ( the primary control of the ANS ). In healthy individuals, the autonomic tone is responsible for restoring homeostasis, the body's ability to maintain a constant internal environment. In dysautonomia, this balance is disturbed, and one or the other branch dominates, causing an overcompensation or withdrawal of the sympathetic or parasympathetic activity.  (4) 

How it all ties together

Since there are so many different ways that the pressure within the blood vessels can be influenced, it is no surprise that a malfunction can have similar symptoms yet completely different causes. Here are a few examples of why different types of dysautonomia cause inappropriate vasodilation or vasoconstriction. (5,6)

Neuropathy

This type of dysautonomia is thought to be caused by the partial denervation of the sympathetic nerves of the lower limbs. Since the smooth muscle cells of the vascular walls respond to the peripheral small fiber nerve endings of the ANS, this denervation may lead to inadequate vasoconstriction. Therefore,  the ANS is unable to prevent or correct blood pooling, leading to a drop in BP and a compensatory increase in heart rate (HR) in response to orthostasis. A study by Jacob et al. showed that patients with neuropathic POTS had normal neuronal norepinephrine release in their arms but less norepinephrine in their lower body.    Meaning there was less sympathetic activation in the blood vessels of the legs. A secondary form of neuropathic dysautonomia occurs in diabetic or alcoholic neuropathy resulting in ineffective blood pressure control via the vascular innervation. (5,6)

Ehler-Danlos Syndrome

Ehlers-Danlos-Syndrome (EDS), or joint hypermobility syndrome, can cause abnormal connective tissue in the vessel walls, which permits the veins to dilate excessively. This dilation causes blood pooling in the lower limbs and a  decrease in blood pressure. Some of these patients also display alpha and beta-adrenergic hyper-responsiveness. (6) 

Mast-Cell Activation

MCAD results in the release of the vasodilator histamine and other mast cell mediators, which may contribute to POTS. The excessive vasodilation caused by this reaction can cause many symptoms consistent with POTS and marked by flushing episodes. (6)

Hyperadrenergic POTS  (HyperPOTS)     

This type of dysautonomia is characterized by an increased level of the neurotransmitter norepinephrine, a vasoconstrictor.  This can occur in several ways: 

  • Sympathetic overcompensation - Norepinephrine gets dumped in response to a drop in BP, possibly due to vasodilation
  • Parasympathetic withdrawal - the ANS fails to counteract sympathetic activation  or the inability to clear excess NE out of the synaptic cleft. 

Hyperadrenergic POTS is often accompanied by high BP, high HR, and symptoms of sudden and extreme vasoconstriction brought on by the "fight-or-flight" response. This can lead to a loss of circulation to the brain and result in syncope or seizures in severe cases. (7)

Neurocardiogenic syncope

The conscious state depends on adequate cerebral blood flow, which is auto-regulated by the ANS. Normal orthostasis is maintained by a brief increase in the sympathetic tone and maintenance of BP.  In neurocardiogenic syncope, there is an inappropriate decrease in sympathetic tone followed by a compensatory increase in parasympathetic tone. This fluctuation leads to a sudden drop in both BP and HR due to vasodilation, often accompanied by a sudden loss of consciousness due to a temporary loss of cerebral circulation. The causes include orthostasis, hot temperature, and emotional triggers.

This article is a brief overview of the intricate and complicated correlation between the ANS and our cardio-vascular system.  Hopefully, this aids in a better understanding of why we experience the symptoms typically experienced with POTS and other forms of dysautonomia. (8)

Sources:

  1. https://biologydictionary.net/vasodilation/
  2. https://healthfully.com/how-do-blood-vessels-constrict-dilate-4240725.html
  3. https://en.wikipedia.org/wiki/Vasoconstriction
  4. https://graduateway.com/chapter-15-the-autonomic-nervous-system-4-essay/
  5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1501099/
  6.  https://www.dinet.org/info/pots/what-causes-pots-r98/
  7. https://www.dinet.org/info/pots/hyperadrenergic-pots-hyperpots-an-overview-of-a-pots-subtype-r220/
  8. https://www.dinet.org/info/ncs/neurocardiogenic-syncope-info-r104/  
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