Efferent Nervous System Drugs and Their Mechanisms of Action

Efferent nervous system drugs are medications specifically designed to target the efferent nervous system. Their modus operandi involves selectively modulating various aspects of nerve impulse transmission and the corresponding receptors, either mimicking or counteracting the effects of specific neurotransmitters. The overarching objective is to alter the functionality of visceral organs or skeletal muscles. These drugs encompass a diverse range, primarily categorized as agonists and antagonists.

Types of Efferent Nervous System Drugs

Agonists:

• Cholinergic agonists (e.g., carbamylcholine, pilocarpine, nicotine)
• Anticholinesterase drugs (e.g., neostigmine)
• Adrenergic agonists (including antagonists such as norepinephrine)

Antagonists:

• Cholinergic antagonists (e.g., atropine, pirenzepine)
• Cholinesterase reactivators (e.g., pralidoxime)
• Adrenergic antagonists (e.g., phentolamine, phenoxybenzamine)

Basic Functions of Efferent Nervous System Drugs

(1) Direct Action on Receptors

Numerous efferent nervous system drugs directly interact with cholinergic or adrenergic receptors, eliciting two distinct responses: agonists mimic the effects of neurotransmitters released from nerve endings, whereas antagonists produce minimal or no agonist-like effects and hinder neurotransmitter binding to receptors, exerting opposing actions.

(2) Impact on Neurotransmitters

a. Affecting neurotransmitter biosynthesis: Bethanechol inhibits acetylcholine biosynthesis, and α-methyltyrosine inhibits norepinephrine biosynthesis. However, these compounds are primarily utilized in pharmacological research rather than clinical settings.

b. Affecting neurotransmitter release: Drugs like ephedrine and metaraminol stimulate norepinephrine (NA) release, while carbachol promotes acetylcholine (ACh) release.

c. Affecting neurotransmitter transport and storage: Certain drugs, such as reserpine, interfere with NA reuptake, functioning as vesicular inhibitors that deplete intracellular NA levels. Desipramine and cocaine also inhibit reuptake.

d. Affecting neurotransmitter metabolism: ACh inactivation relies heavily on cholinesterase hydrolysis. Consequently, cholinesterase inhibitors disrupt ACh metabolism, leading to ACh accumulation in the body and producing subsequent effects.