CHAPTER-2
DRUGS ACTING ON THE PERIPHERAL NERVOUS SYSTEM
The Peripheral Nervous System (PNS) is a complex network of nerves that extends outside
the brain and spinal cord, connecting the Central Nervous System (CNS) to the rest of the
body. It plays a crucial role in both voluntary movements and involuntary bodily functions.
Drugs acting on the PNS typically target specific receptors or enzymes within its two main
divisions: the Autonomic Nervous System (ANS) and the Somatic Nervous System (SNS).
I. Drugs Acting on the Autonomic Nervous System (ANS)
The ANS controls involuntary bodily functions like heart rate, digestion, respiration, and
blood pressure. It is further divided into the Sympathetic Nervous System (SNS) and the
Parasympathetic Nervous System (PNS), which generally have opposing effects to
maintain homeostasis.
A. Drugs Affecting the Sympathetic Nervous System (Adrenergic Drugs)
The primary neurotransmitters in the sympathetic nervous system are norepinephrine
(noradrenaline) and epinephrine (adrenaline), which act on adrenergic receptors (alpha (α)
and beta (β)).
Sympathomimetics (Adrenergic Agonists): These drugs mimic or enhance the effects of
sympathetic stimulation.
Mechanism: Directly activate adrenergic receptors or indirectly increase the release of
norepinephrine.
Examples and Uses:
Alpha-1 Agonists: Phenylephrine, Pseudoephedrine (vasoconstriction, nasal decongestion,
increase blood pressure).
Alpha-2 Agonists: Clonidine (reduce CNS sympathetic outflow, used for hypertension,
ADHD).
,Beta-1 Agonists: Dobutamine (increase heart rate and contractility, used in heart failure,
cardiac arrest).
Beta-2 Agonists: Albuterol, Salbutamol (bronchodilation, used for asthma, COPD).
Non-selective Agonists: Epinephrine (acts on α and β receptors, used in anaphylaxis,
cardiac arrest), Norepinephrine (primarily α-agonist, used for septic shock).
Sympatholytics (Adrenergic Antagonists/Blockers): These drugs block or reduce the
effects of sympathetic stimulation.
Mechanism: Block adrenergic receptors, inhibit norepinephrine synthesis/release, or
deplete norepinephrine stores.
Examples and Uses:
Alpha-1 Blockers: Prazosin, Tamsulosin (vasodilation, lower blood pressure, improve
urine flow in benign prostatic hyperplasia).
Beta Blockers:
Non-selective Beta Blockers: Propranolol (reduce heart rate and blood pressure, used for
hypertension, angina, migraines, anxiety).
Selective Beta-1 Blockers: Metoprolol, Atenolol (primarily reduce heart rate and blood
pressure, safer for patients with asthma/COPD).
B. Drugs Affecting the Parasympathetic Nervous System (Cholinergic Drugs)
The primary neurotransmitter in the parasympathetic nervous system is acetylcholine
(ACh), which acts on cholinergic receptors (muscarinic and nicotinic).
Parasympathomimetics (Cholinergic Agonists): These drugs mimic or enhance the
effects of parasympathetic stimulation.
Mechanism: Directly activate cholinergic receptors or indirectly inhibit
acetylcholinesterase (enzyme that breaks down ACh), thus increasing ACh levels.
,Examples and Uses:
Direct-acting Muscarinic Agonists: Pilocarpine (constrict pupils, increase
salivation/sweating, used for glaucoma, dry mouth). Bethanechol (stimulate bladder
contraction, used for urinary retention).
Indirect-acting Cholinesterase Inhibitors: Neostigmine, Pyridostigmine (increase ACh
at neuromuscular junction, used for myasthenia gravis, reversal of neuromuscular
blockade). Donepezil, Rivastigmine (increase ACh in CNS, used for Alzheimer's disease).
Parasympatholytics (Cholinergic Antagonists/Blockers/Antimuscarinics): These drugs
block or reduce the effects of parasympathetic stimulation.
Mechanism: Block cholinergic receptors, primarily muscarinic receptors.
Examples and Uses:
Muscarinic Antagonists: Atropine (dilate pupils, decrease secretions, increase heart rate,
antidote for organophosphate poisoning). Scopolamine (prevent motion sickness, reduce
GI motility). Oxybutynin (relax overactive bladder). Ipratropium (bronchodilation, used for
COPD, asthma).
II. Drugs Acting on the Somatic Nervous System (SNS)
The SNS controls voluntary movements by innervating skeletal muscles. The primary
neurotransmitter at the neuromuscular junction (where nerves meet muscles) is
acetylcholine, acting on nicotinic receptors.
Neuromuscular Blockers: These drugs interfere with the transmission of nerve impulses
at the neuromuscular junction, leading to muscle paralysis. They are crucial in surgical
anesthesia to facilitate intubation and muscle relaxation during procedures.
Mechanism:
Non-depolarizing Blockers: Compete with ACh for nicotinic receptors at the motor end
plate, preventing depolarization. (e.g., Vecuronium, Rocuronium, Atracurium,
Pancuronium). Effects can be reversed by cholinesterase inhibitors.
, Depolarizing Blockers: Act as agonists at nicotinic receptors, causing initial
depolarization followed by sustained depolarization that prevents further muscle
contraction. (e.g., Succinylcholine). This leads to transient muscle fasciculations followed
by paralysis. Rapid onset and short duration.
Skeletal Muscle Relaxants (Centrally Acting): These drugs typically act on the CNS to
reduce muscle spasms and spasticity, rather than directly at the neuromuscular junction.
While their primary site of action is central, their effects manifest as peripheral muscle
relaxation.
Mechanism: Many enhance GABAergic inhibition in the spinal cord or brainstem.
Examples and Uses: Diazepam (benzodiazepine), Baclofen, Tizanidine, Cyclobenzaprine
(used for muscle spasms, spasticity in conditions like multiple sclerosis, spinal cord
injury).
Local Anesthetics: These drugs temporarily block nerve impulse transmission in a specific
area, leading to loss of sensation without affecting consciousness.
Mechanism: Block voltage-gated sodium channels in nerve membranes, preventing the
generation and propagation of action potentials.
Examples and Uses: Lidocaine, Bupivacaine, Procaine (used for regional anesthesia, pain
relief, dental procedures, topical numbness).
Understanding how these drugs interact with the different components of the PNS is
essential for their safe and effective therapeutic use in a wide range of conditions, from
managing blood pressure and asthma to facilitating surgery and treating pain.
STEPS INVOLVED IN NEUROHUMORAL TRANSMISSION
Neurohumoral transmission is the process by which nerve impulses are transmitted across a
synapse or a neuroeffector junction (where a nerve meets a muscle or gland) by the release
DRUGS ACTING ON THE PERIPHERAL NERVOUS SYSTEM
The Peripheral Nervous System (PNS) is a complex network of nerves that extends outside
the brain and spinal cord, connecting the Central Nervous System (CNS) to the rest of the
body. It plays a crucial role in both voluntary movements and involuntary bodily functions.
Drugs acting on the PNS typically target specific receptors or enzymes within its two main
divisions: the Autonomic Nervous System (ANS) and the Somatic Nervous System (SNS).
I. Drugs Acting on the Autonomic Nervous System (ANS)
The ANS controls involuntary bodily functions like heart rate, digestion, respiration, and
blood pressure. It is further divided into the Sympathetic Nervous System (SNS) and the
Parasympathetic Nervous System (PNS), which generally have opposing effects to
maintain homeostasis.
A. Drugs Affecting the Sympathetic Nervous System (Adrenergic Drugs)
The primary neurotransmitters in the sympathetic nervous system are norepinephrine
(noradrenaline) and epinephrine (adrenaline), which act on adrenergic receptors (alpha (α)
and beta (β)).
Sympathomimetics (Adrenergic Agonists): These drugs mimic or enhance the effects of
sympathetic stimulation.
Mechanism: Directly activate adrenergic receptors or indirectly increase the release of
norepinephrine.
Examples and Uses:
Alpha-1 Agonists: Phenylephrine, Pseudoephedrine (vasoconstriction, nasal decongestion,
increase blood pressure).
Alpha-2 Agonists: Clonidine (reduce CNS sympathetic outflow, used for hypertension,
ADHD).
,Beta-1 Agonists: Dobutamine (increase heart rate and contractility, used in heart failure,
cardiac arrest).
Beta-2 Agonists: Albuterol, Salbutamol (bronchodilation, used for asthma, COPD).
Non-selective Agonists: Epinephrine (acts on α and β receptors, used in anaphylaxis,
cardiac arrest), Norepinephrine (primarily α-agonist, used for septic shock).
Sympatholytics (Adrenergic Antagonists/Blockers): These drugs block or reduce the
effects of sympathetic stimulation.
Mechanism: Block adrenergic receptors, inhibit norepinephrine synthesis/release, or
deplete norepinephrine stores.
Examples and Uses:
Alpha-1 Blockers: Prazosin, Tamsulosin (vasodilation, lower blood pressure, improve
urine flow in benign prostatic hyperplasia).
Beta Blockers:
Non-selective Beta Blockers: Propranolol (reduce heart rate and blood pressure, used for
hypertension, angina, migraines, anxiety).
Selective Beta-1 Blockers: Metoprolol, Atenolol (primarily reduce heart rate and blood
pressure, safer for patients with asthma/COPD).
B. Drugs Affecting the Parasympathetic Nervous System (Cholinergic Drugs)
The primary neurotransmitter in the parasympathetic nervous system is acetylcholine
(ACh), which acts on cholinergic receptors (muscarinic and nicotinic).
Parasympathomimetics (Cholinergic Agonists): These drugs mimic or enhance the
effects of parasympathetic stimulation.
Mechanism: Directly activate cholinergic receptors or indirectly inhibit
acetylcholinesterase (enzyme that breaks down ACh), thus increasing ACh levels.
,Examples and Uses:
Direct-acting Muscarinic Agonists: Pilocarpine (constrict pupils, increase
salivation/sweating, used for glaucoma, dry mouth). Bethanechol (stimulate bladder
contraction, used for urinary retention).
Indirect-acting Cholinesterase Inhibitors: Neostigmine, Pyridostigmine (increase ACh
at neuromuscular junction, used for myasthenia gravis, reversal of neuromuscular
blockade). Donepezil, Rivastigmine (increase ACh in CNS, used for Alzheimer's disease).
Parasympatholytics (Cholinergic Antagonists/Blockers/Antimuscarinics): These drugs
block or reduce the effects of parasympathetic stimulation.
Mechanism: Block cholinergic receptors, primarily muscarinic receptors.
Examples and Uses:
Muscarinic Antagonists: Atropine (dilate pupils, decrease secretions, increase heart rate,
antidote for organophosphate poisoning). Scopolamine (prevent motion sickness, reduce
GI motility). Oxybutynin (relax overactive bladder). Ipratropium (bronchodilation, used for
COPD, asthma).
II. Drugs Acting on the Somatic Nervous System (SNS)
The SNS controls voluntary movements by innervating skeletal muscles. The primary
neurotransmitter at the neuromuscular junction (where nerves meet muscles) is
acetylcholine, acting on nicotinic receptors.
Neuromuscular Blockers: These drugs interfere with the transmission of nerve impulses
at the neuromuscular junction, leading to muscle paralysis. They are crucial in surgical
anesthesia to facilitate intubation and muscle relaxation during procedures.
Mechanism:
Non-depolarizing Blockers: Compete with ACh for nicotinic receptors at the motor end
plate, preventing depolarization. (e.g., Vecuronium, Rocuronium, Atracurium,
Pancuronium). Effects can be reversed by cholinesterase inhibitors.
, Depolarizing Blockers: Act as agonists at nicotinic receptors, causing initial
depolarization followed by sustained depolarization that prevents further muscle
contraction. (e.g., Succinylcholine). This leads to transient muscle fasciculations followed
by paralysis. Rapid onset and short duration.
Skeletal Muscle Relaxants (Centrally Acting): These drugs typically act on the CNS to
reduce muscle spasms and spasticity, rather than directly at the neuromuscular junction.
While their primary site of action is central, their effects manifest as peripheral muscle
relaxation.
Mechanism: Many enhance GABAergic inhibition in the spinal cord or brainstem.
Examples and Uses: Diazepam (benzodiazepine), Baclofen, Tizanidine, Cyclobenzaprine
(used for muscle spasms, spasticity in conditions like multiple sclerosis, spinal cord
injury).
Local Anesthetics: These drugs temporarily block nerve impulse transmission in a specific
area, leading to loss of sensation without affecting consciousness.
Mechanism: Block voltage-gated sodium channels in nerve membranes, preventing the
generation and propagation of action potentials.
Examples and Uses: Lidocaine, Bupivacaine, Procaine (used for regional anesthesia, pain
relief, dental procedures, topical numbness).
Understanding how these drugs interact with the different components of the PNS is
essential for their safe and effective therapeutic use in a wide range of conditions, from
managing blood pressure and asthma to facilitating surgery and treating pain.
STEPS INVOLVED IN NEUROHUMORAL TRANSMISSION
Neurohumoral transmission is the process by which nerve impulses are transmitted across a
synapse or a neuroeffector junction (where a nerve meets a muscle or gland) by the release
