And I will make it even easier by getting rid of the nicotinic receptors after I tell you they are involved in muscle contraction and are affected by substances such as curare used on those poison-tipped arrows that cause muscle paralysis by blocking these nicotinic receptors. Medications such as succinlycholine are available to block the nicotinic receptors and induce paralysis necessary for certain medical procedures. We are left with the one parasympathetic receptor you must learn, the muscarinic receptor.
When this receptor is stimulated, it causes a decrease in the heart rate, a decrease in heart contractility and a decrease in the size of the bronchioles. When we are at rest, we can slow down and conserve energy. The parasympathetic nervous system helps us do this. What would happen if we block the muscarinic receptors?
That would cause the heart rate and contractility to increase, dilation of the bronchioles and less production of secretions in the body. This is the exact effect of atropine, a drug we use to counteract too much parasympathetic activity such as from over-stimulation of the vagus nerve or the effects of certain chemical warfare nerve agents and organophosphate poisoning. Atropine is a parasympatholytic, we can also call it a parasympathetic antagonist or parasympathetic blocker or an anticholinergic medication.
All these terms mean the same; it means they block the action of acetylcholine at the parasympathetic receptors. The effect of blocking any receptor causes the opposite effect we would expect from stimulating the receptor. Ipratroprium is another example of a parasympathetic blocker medication but this one is inhaled so most of the effect occurs in the lungs, and when we block parasympathetic receptors in the lungs we cause the bronchioles to dilate and decrease production of secretions like mucus.
That makes ipratroprium useful in the patient with COPD who produces excessive pulmonary mucous and in combination with albuterol for any wheezing patient.
But remember that the primary rescue medication for bronchospasm is a beta 2 agoinist such as albuterol although ipratrorium is often added and is available as a combination inhaler with albuterol called Combivent. It is important to remember that it is the balance between the sympathetic and parasympathetic nervous system that keeps our automated body functions in balance and working properly. Outside forces, including drugs, medications or poisons can change the functioning of the autonomic nervous system.
And it is wise to keep in mind that all medications are potential toxins that have some beneficial side effects. In summary, if you are familiar with the actions of the autonomic nervous system receptors then you can easily recall the therapeutic actions of many commonly used medications and their overdose presentation as well as certain poisons and frequently abused drugs. Test your knowledge of the autonomic nervous system with EMS1's quiz and add your comments below.
Looking for more clinical education articles? Become an EMS1 member to receive helpful tips and resources delivered to your inbox. He is a Montana licensed paramedic and physician. Since , he has been the medical director for Big Horn County Montana, which currently provides Advanced Life Support response and critical care interfacility transports for a large geographic area.
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Documented effects of beta 2-adrenergic receptor activation in the human lung include smooth muscle relaxation, inhibition of acetylcholine release from cholinergic nerve terminals, stimulation of serous and mucous cell secretion, increases in ciliary beat frequency, promotion of water movement into the airway lumen by stimulation of ion secretion across the apical membrane of epithelial cells, increase in bronchial blood flow, reduction in venular permeability, and inhibition of mediator release from some, but not all, inflammatory cells.
Beta 2-Adrenergic receptors are present in normal or increased numbers on asthmatic airway smooth muscle but are uncoupled in severe asthma, leading to functional hyporesponsiveness, probably due to the effects of inflammatory mediators. There is also evidence for dysfunction of beta 2-adrenergic receptors on circulating inflammatory cells following mediator release.
However, dysfunction of the receptors on airway smooth muscle and inflammatory cells is unlikely to be of primary importance in the pathogenesis of asthma. There is increasing concern that regular beta 2-adrenergic receptor agonist use in the therapy of asthma is deleterious. Although a number of theories have been advanced to explain such an effect, none is well established and further research is urgently required.
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