Week 2: Overview of Peripheral Nervous System Drugs and
Drugs Affecting the Cardiovascular System (Part 1)
Week 2, Module 1 (Overview of Peripheral Nervous System) Objectives:
1. Identify the two major divisions of the peripheral nervous system.
2. Differentiate between the sympathetic and parasympathetic branches of the autonomic nervous
system.
3. Differentiate between the four main subtypes of adrenergic receptors: alpha1, alpha2, beta1, and beta2.
4. Differentiate between the three main subtypes of cholinergic receptors: nicotinicN, nicotinicM, and
muscarinic.
5. Identify the basic processes by which the main autonomic nervous system neurotransmitters are
terminated physiologically.
6. Describe the actions of various drugs on nicotinic, muscarinic, and adrenergic receptors in the
peripheral nervous system.
Week 2, Module 1 Chapters
● Chapter 11 | Basic Principles of Neuropharmacology
● Chapter 12 | Physiology of the Peripheral Nervous System
● Chapter 13 | Muscarinic Agonists and Cholinesterase Inhibitors
● Chapter 14 | Muscarinic Antagonists
● Chapter 15 | Adrenergic Agonists
● Chapter 16 | Adrenergic Antagonists
● Chapter 17 | Indirect-Acting Antiadrenergic Agents
,Chapter 11: Basic Principles of Neuropharmacology
● Neuropharmacology is the study of drugs that alter processes controlled by the nervous system
● These drugs are used to treat conditions that range from depression to epilepsy to hypertension to
asthma (produce effects equal to those produced by excitation/suppression of neuronal activity)
● Neuropharmacologic agents can be divided into two broad categories:
➢ Peripheral nervous system drugs
➢ Central nervous system drugs
● Axonal conduction- the process of conducting an action potential down the axon of the neuron
● Synaptic transmission- the process by which information is carried across the gap between the
neuron and the postsynaptic cell; requires release of neurotransmitters from axon terminal followed by
binding of these molecules to receptors on the postsynaptic cell → change in cell behavior
➢ Step 1: Transmitter Synthesis- molecules from which transmitter is made must be present in
nerve terminal for synaptic transmission to take place
➢ Step 2: Transmitter Storage- after synthesis, transmitter is stored within vesicles in the axon
terminal
➢ Step 3: Transmitter Release- triggered by arrival of action potential at the axon terminal;
vesicles undergo fusion with terminal membrane & contents release into synaptic gap; each
AP causes only a small fraction of vesicles to discharge contents
➢ Step 4: Receptor Binding- transmitter molecules diffuse across synaptic gap and undergo
reversible binding to receptors on postsynaptic cell; this initiates cascade of events that alters
behavior in postsynaptic cell
➢ Step 5: Termination of Transmission- by dissociation of transmitter from receptors and then
removal of free transmitter from synaptic gap; can be removed by 3 processes
➔ Reuptake- axon terminals contain pumps that transport transmitter back into neuron
from which they were released; transmitter may then be degraded or packaged in
vesicles for reuse
➔ Enzymatic Degradation- synapse contains large quantities of transmitter-inactivating
enzymes
➔ Diffusion- away from synaptic gap, but is very slow and not significant
Basic Mechanisms of Neuropharmacologic Agents
● Most neuropharm agents act by altering synaptic transmission, which are more selective than those
altering axonal conduction
● The effect of a drug on a neuronally regulated process is dependent on the ability of that drug to
directly or indirectly influence receptor activity on target cells
,● When a drug influences receptor function, it can either enhance receptor activation (mimic transmitter
effects) or reduce receptor activation (opposite)
● Axonal conduction- not very selective
➢ Local anesthetics- produce nonselective inhibition of axonal conduction and suppress
transmission in any nerve they reach
● Synaptic transmission- can produce effects that are highly selective; synapses at different sites employ
different transmitters, the body employs more than one type of receptor for most transmitters
➢ Transmitter synthesis
➔ Increase transmitter synthesis (more T) → increase receptor activation
➔ Decrease transmitter synthesis (less T) → decrease receptor activation
➔ Synthesis of transmitter molecules that are more effective than the transmitter itself
(drugs converted into “super” transmitters) → increase receptor activation
➢ Transmitter storage
➔ Reduced storage (less T) → decrease receptor activation
➢ Transmitter release
➔ Promote T release → increase receptor activation (Amphetamines)
➔ Inhibit T release → decrease receptor activation (Botox)
➢ Receptor binding
➔ Direct receptor activation (bind to receptor and activate; agonists) →increase
receptor activation (morphine, epinephrine, insulin)
➔ Blockade of T binding (bind to receptor and block activation; antagonists) →
decrease receptor activation (naloxone, antihistamines, metoprolol)
➔ Enhanced response to T (bind to receptor components to enhance the natural
transmitter) → increase receptor activation (benzodiazepines-valium)
➢ Termination of transmission
➔ Blockade of T reuptake (increase T availability) → increase receptor activation
➔ Inhibition of T breakdown (increase T availability) → increase receptor activation
● Receptor types and selectivity of drug action- Mort & Merv: the more types of receptors we have to
work with, the greater our chances of producing selective drug effects
● Peripheral nervous symptom drugs- to understand them, you need to know:
1. The type/s of receptor through which the drug acts
2. The normal response to activation of those receptors
3. What the drug does to receptor function
Ex: Isoproterenol
, Chapter 12: Physiology of the Peripheral Nervous System
Divisions of the Nervous System
● Central nervous system
➢ Brain and spinal cord
● Peripheral nervous system
➢ Somatic motor system- controls voluntary movement of muscles
➢ Autonomic nervous system (ANS) - regulate many involuntary processes; regulation of the
heart, secretory glands (salivary, gastric, sweat, bronchial glands), and smooth muscles
(bronchi, blood vessels, urogenital system, and GI tract)
• Parasympathetic nervous system- 7 regulatory functions- stimulation causes slowing of
HR, increased gastric secretion, emptying of bladder, emptying of bowel, focusing the eye for
near vision, constricting the pupil, contracting bronchial smooth muscle; “housekeeping
chores” of the body, conserves energy
➔ Meds used primarily for their effects of GI tract, bladder, and eye; occasionally used
for effects on HR and lungs
➔ Poisons block PNS (insecticides, nerve gases)
• Sympathetic nervous system- 3 main functions- regulating cardiovascular system,
regulating body temp, and implementing the acute stress response (fight or flight); stimulation
to heart increases CO, to arterioles/veins causes vasoconstriction; can achieve maintenence of
blood flow to brain, redistribution of blood flow during exercise, compensation for blood
loss; regulates body temp (sweat, piloerection)
➔ Fight/flight response- increasing HR and BP, shunting blood from skin and viscera
into skeletal muscles, dilating bronchi to improve oxygenation, dilating pupils
(enhance vision), mobilizing stored energy (glucose for brain and fatty acids for
muscles)
➔ Meds used are mainly for effects on heart, blood vessels, and lungs (HTN, HF,
angina pectoris, asthma)
Normal Regulation of ANS
● Feedback regulation
● Baroreceptor reflex- regulates BP
● Autonomic tone
Drugs Affecting the Cardiovascular System (Part 1)
Week 2, Module 1 (Overview of Peripheral Nervous System) Objectives:
1. Identify the two major divisions of the peripheral nervous system.
2. Differentiate between the sympathetic and parasympathetic branches of the autonomic nervous
system.
3. Differentiate between the four main subtypes of adrenergic receptors: alpha1, alpha2, beta1, and beta2.
4. Differentiate between the three main subtypes of cholinergic receptors: nicotinicN, nicotinicM, and
muscarinic.
5. Identify the basic processes by which the main autonomic nervous system neurotransmitters are
terminated physiologically.
6. Describe the actions of various drugs on nicotinic, muscarinic, and adrenergic receptors in the
peripheral nervous system.
Week 2, Module 1 Chapters
● Chapter 11 | Basic Principles of Neuropharmacology
● Chapter 12 | Physiology of the Peripheral Nervous System
● Chapter 13 | Muscarinic Agonists and Cholinesterase Inhibitors
● Chapter 14 | Muscarinic Antagonists
● Chapter 15 | Adrenergic Agonists
● Chapter 16 | Adrenergic Antagonists
● Chapter 17 | Indirect-Acting Antiadrenergic Agents
,Chapter 11: Basic Principles of Neuropharmacology
● Neuropharmacology is the study of drugs that alter processes controlled by the nervous system
● These drugs are used to treat conditions that range from depression to epilepsy to hypertension to
asthma (produce effects equal to those produced by excitation/suppression of neuronal activity)
● Neuropharmacologic agents can be divided into two broad categories:
➢ Peripheral nervous system drugs
➢ Central nervous system drugs
● Axonal conduction- the process of conducting an action potential down the axon of the neuron
● Synaptic transmission- the process by which information is carried across the gap between the
neuron and the postsynaptic cell; requires release of neurotransmitters from axon terminal followed by
binding of these molecules to receptors on the postsynaptic cell → change in cell behavior
➢ Step 1: Transmitter Synthesis- molecules from which transmitter is made must be present in
nerve terminal for synaptic transmission to take place
➢ Step 2: Transmitter Storage- after synthesis, transmitter is stored within vesicles in the axon
terminal
➢ Step 3: Transmitter Release- triggered by arrival of action potential at the axon terminal;
vesicles undergo fusion with terminal membrane & contents release into synaptic gap; each
AP causes only a small fraction of vesicles to discharge contents
➢ Step 4: Receptor Binding- transmitter molecules diffuse across synaptic gap and undergo
reversible binding to receptors on postsynaptic cell; this initiates cascade of events that alters
behavior in postsynaptic cell
➢ Step 5: Termination of Transmission- by dissociation of transmitter from receptors and then
removal of free transmitter from synaptic gap; can be removed by 3 processes
➔ Reuptake- axon terminals contain pumps that transport transmitter back into neuron
from which they were released; transmitter may then be degraded or packaged in
vesicles for reuse
➔ Enzymatic Degradation- synapse contains large quantities of transmitter-inactivating
enzymes
➔ Diffusion- away from synaptic gap, but is very slow and not significant
Basic Mechanisms of Neuropharmacologic Agents
● Most neuropharm agents act by altering synaptic transmission, which are more selective than those
altering axonal conduction
● The effect of a drug on a neuronally regulated process is dependent on the ability of that drug to
directly or indirectly influence receptor activity on target cells
,● When a drug influences receptor function, it can either enhance receptor activation (mimic transmitter
effects) or reduce receptor activation (opposite)
● Axonal conduction- not very selective
➢ Local anesthetics- produce nonselective inhibition of axonal conduction and suppress
transmission in any nerve they reach
● Synaptic transmission- can produce effects that are highly selective; synapses at different sites employ
different transmitters, the body employs more than one type of receptor for most transmitters
➢ Transmitter synthesis
➔ Increase transmitter synthesis (more T) → increase receptor activation
➔ Decrease transmitter synthesis (less T) → decrease receptor activation
➔ Synthesis of transmitter molecules that are more effective than the transmitter itself
(drugs converted into “super” transmitters) → increase receptor activation
➢ Transmitter storage
➔ Reduced storage (less T) → decrease receptor activation
➢ Transmitter release
➔ Promote T release → increase receptor activation (Amphetamines)
➔ Inhibit T release → decrease receptor activation (Botox)
➢ Receptor binding
➔ Direct receptor activation (bind to receptor and activate; agonists) →increase
receptor activation (morphine, epinephrine, insulin)
➔ Blockade of T binding (bind to receptor and block activation; antagonists) →
decrease receptor activation (naloxone, antihistamines, metoprolol)
➔ Enhanced response to T (bind to receptor components to enhance the natural
transmitter) → increase receptor activation (benzodiazepines-valium)
➢ Termination of transmission
➔ Blockade of T reuptake (increase T availability) → increase receptor activation
➔ Inhibition of T breakdown (increase T availability) → increase receptor activation
● Receptor types and selectivity of drug action- Mort & Merv: the more types of receptors we have to
work with, the greater our chances of producing selective drug effects
● Peripheral nervous symptom drugs- to understand them, you need to know:
1. The type/s of receptor through which the drug acts
2. The normal response to activation of those receptors
3. What the drug does to receptor function
Ex: Isoproterenol
, Chapter 12: Physiology of the Peripheral Nervous System
Divisions of the Nervous System
● Central nervous system
➢ Brain and spinal cord
● Peripheral nervous system
➢ Somatic motor system- controls voluntary movement of muscles
➢ Autonomic nervous system (ANS) - regulate many involuntary processes; regulation of the
heart, secretory glands (salivary, gastric, sweat, bronchial glands), and smooth muscles
(bronchi, blood vessels, urogenital system, and GI tract)
• Parasympathetic nervous system- 7 regulatory functions- stimulation causes slowing of
HR, increased gastric secretion, emptying of bladder, emptying of bowel, focusing the eye for
near vision, constricting the pupil, contracting bronchial smooth muscle; “housekeeping
chores” of the body, conserves energy
➔ Meds used primarily for their effects of GI tract, bladder, and eye; occasionally used
for effects on HR and lungs
➔ Poisons block PNS (insecticides, nerve gases)
• Sympathetic nervous system- 3 main functions- regulating cardiovascular system,
regulating body temp, and implementing the acute stress response (fight or flight); stimulation
to heart increases CO, to arterioles/veins causes vasoconstriction; can achieve maintenence of
blood flow to brain, redistribution of blood flow during exercise, compensation for blood
loss; regulates body temp (sweat, piloerection)
➔ Fight/flight response- increasing HR and BP, shunting blood from skin and viscera
into skeletal muscles, dilating bronchi to improve oxygenation, dilating pupils
(enhance vision), mobilizing stored energy (glucose for brain and fatty acids for
muscles)
➔ Meds used are mainly for effects on heart, blood vessels, and lungs (HTN, HF,
angina pectoris, asthma)
Normal Regulation of ANS
● Feedback regulation
● Baroreceptor reflex- regulates BP
● Autonomic tone
