The parasympathetic nervous system (PSNS) is responsible for conserving energy and promoting restorative processes. It slows the heart rate, stimulates digestion, and promotes glandular secretions. The primary neurotransmitter of the PSNS is acetylcholine, which acts on cholinergic receptors.

In contrast, the sympathetic nervous system (SNS) prepares the body for stress or emergencies. It increases heart rate, dilates airways, and redirects blood flow to muscles. The SNS primarily uses norepinephrine and epinephrine as neurotransmitters, which act on adrenergic receptors.

While the PSNS and SNS often have opposing effects, they work together to regulate vital functions. For example, the PSNS slows the heart rate, while the SNS increases it, allowing the body to adapt to different situations. The two primary neurotransmitters of the ANS:

• Acetylcholine (ACh) – Acetylcholine is the neurotransmitter of the PSNS and is released by both preganglionic and postganglionic neurons. It acts on nicotinic receptors (at ganglia) and muscarinic receptors (at target organs).

• Norepinephrine (NE) – Norepinephrine is the primary neurotransmitter of the SNS and is released by postganglionic neurons. It acts on adrenergic receptors (alpha and beta subtypes) at target organs.

Epinephrine, a hormone released by the adrenal medulla, also acts on adrenergic receptors and amplifies the effects of the SNS. The effects of the ANS are mediated by specific receptor types, which are divided into cholinergic and adrenergic receptors.

Cholinergic Receptors

• Nicotinic Receptors: 

• • Found at the ganglia of both the PSNS and SNS.
  • These are ionotropic receptors, meaning they function as ion channels that open upon activation, allowing ions like sodium and calcium to flow into the cell.
  • Nicotinic receptors are responsible for the rapid transmission of signals between neurons.

• Muscarinic Receptors: 

• • Found at the target organs of the PSNS.
  • These are metabotropic receptors, meaning they are G-protein-coupled receptors that activate second messenger systems. Subtypes include: 

• • • M2: Found in the heart; decreases heart rate and conduction.
    • M3: Found in smooth muscle and glands; promotes smooth muscle contraction (e.g., in the bladder) and glandular secretion (e.g., saliva).

Adrenergic Receptors

• Alpha Receptors: 

• • Alpha-1: Found in blood vessels; causes vasoconstriction, increasing blood pressure. 
  • Alpha-2: Found in presynaptic neurons; inhibits norepinephrine release, providing negative feedback.

• Beta Receptors: 

• • Beta-1: Found in the heart; increases heart rate, contractility, and conduction.
  • Beta-2: Found in smooth muscle (e.g., bronchioles); causes relaxation, leading to bronchodilation.

Cholinergic agonists mimic the effects of acetylcholine, stimulating the PSNS. Examples include

Pilocarpine, a muscarinic agonist used to treat xerostomia (dry mouth) by stimulating salivary gland secretion. It is also used in the treatment of glaucoma to reduce intraocular pressure by contracting the ciliary muscle.

Adrenergic agonists mimic the effects of norepinephrine and epinephrine, stimulating the SNS.

Examples include Epinephrine, used in emergency situations, such as anaphylaxis, to stimulate alpha and beta receptors.It causes vasoconstriction (via alpha-1 receptors) and bronchodilation (via beta-2 receptors). Epinephrine is commonly added to local anesthetics to prolong their duration of action. Epinephrine causes vasoconstriction by stimulating alpha-1 receptors in blood vessels. This reduces blood flow at the injection site, slowing the absorption of the anesthetic into the bloodstream and prolonging its effect. Epinephrine can also reduce systemic toxicity, and improve hemostasis by reducing localized bleeding. Epinephrine reversal occurs when an alpha-blocker (e.g., phentolamine) is administered, blocking the vasoconstrictive effects of epinephrine. This unopposed beta-2 receptor activation leads to vasodilation and a drop in blood pressure.

Beta-blockers are adrenergic antagonists that block beta receptors, reducing the effects of the SNS.

Examples include Propranolol, a non-selective beta-blocker that reduces heart rate and blood pressure by blocking beta-1 receptors in the heart. It is used to treat hypertension, angina, and certain arrhythmias.

Vasovagal syncope, or fainting, occurs due to excessive activation of the PSNS, leading to a sudden drop in heart rate and blood pressure. If this occurs, place the patient in a supine position with their legs elevated to improve blood flow to the brain. Though this is most likely the only intervention required, you can administer atropine (a muscarinic antagonist) if necessary to block excessive vagal stimulation and restore heart rate.