4. Introduction to the nervous
system
The nervous system is divided into two
anatomical divisions:
1. the central nervous system (CNS),
which is composed of the brain and
spinal cord.
2. the peripheral nervous system,
which includes neurons located
outside the brain and spinal cord
5. Cont’
the peripheral nervous system
subdivided into
1. Afferent division : is important in the
reflex regulation .
sensory nerve carrying sensory
information from the receptor to the CNS
1. Efferent division : The ANS carries
nerve impulses from the CNS to the
effector organs
Motor nerve carrying the motor commands
from the CNS to the effectors
by way of two types of efferent neurons:
the preganglionic neurons and the
postganglionic neurons
7. Somatic and Autonomic nervous
systems
Efferent neuron subdivided into :
1. Somatic nervous system
voluntary , stimulate skeletal muscle
2. Autonomic nervous system (ANS)
involuntary , stimulate cardiac muscles ,
muscles and glands and is subdivided
into
1. Parasympathetic
2. Sympathetic
3. Enteric
8.
9.
10. Somatic nervous system
Somatic (voluntary) neurons
exit all levels of the brain and spinal cord (CNS).
Neurotransmitter : acetylcholine (Ach)
Targeted receptor : activate nicotinic receptors (Nm) on
skeletal muscle.
no ganglia
11. Autonomic nervous system
(ANS)
1. Parasympathetic nervous system :
Preganglionic is exit the brain and sacral spinal cord
where they synapse with ganglia near smooth muscle
and heart
Neurotransmitter : acetylcholine (Ach)
Targeted receptor : activates nicotinic receptors (Nn)
on postganglionic neurons
Postganglionic
Neurotransmitter: acetylcholine (Ach)
Targeted receptor : activate muscarinic receptors (M)
on the target tissues (smooth muscle and heart)
12. Autonomic nervous system
(ANS)
2. Sympathetic nervous system :
Preganglionic exit the thoracic and lumbar levels
(thoracolumbar) of the spinal cord and synapse with ganglia
near the cord
Neurotransmitter : acetylcholine (Ach)
Targeted receptor : activate (Nn) receptors on postganglionic
neurons.
Postganglionic
Neurotransmitter : norepinephrine (NE)
Targeted receptor : activate alpha and beta receptors (α, β).
Neurotransmitter: acetylcholine (Ach)
Targeted receptor: activates muscarinic receptors (M)of the
sweat glands.
Targeted receptor: stimulate the adrenal medulla and release
the epinephrine activate alpha and beta receptors (α, β).
13. Action of Sympathetic and
Parasympathetic
Sympathetic nervous system the changes
experienced by the body during emergencies are
referred to as the “fight or flight” response
Parasympathetic nervous system usually acts to
oppose or balance the actions of the sympathetic
division which is referred to as the “rest-and-digest”
situations
21. Divide Autonomic Pharmacology information to four
categories:
Drugs that increase the sympathetic nervous system
response (Sympathomimetic, adrenergic, adrenergic
agonists).
Drugs that increase the parasympathetic nervous system
response (parasympathomimetic, cholinergic, cholinergic
agonists).
Drugs that block the sympathetic nervous system
response (Sympatholytic, antiadrenergic,
adrenergic antagonists).
Drugs that block the parasympathetic nervous system
22. SYMATHETIC AGONIST SAME EFFECT AS
PARASYMPATHETIC ANTAGONIST
SYMATHETIC ANTAGONIST SAME EFFECT AS
PARASYMPATHETIC AGONIST
25. Definitions
Cholinergic Agonists:
Drugs that mimic the effects of ACh by binding directly to
cholinoceptors (muscarinic or nicotinic).
Ach is the main neurotransmitter in the parasympathetic
nerve system.
Cholinergic drugs promote the action of the
neurotransmitter acetylcholine.
Drugs that produce actions similar to stimulate the
parasympathetic nervous system response
(parasympathomimetic, cholinergic, cholinergic agonists).
27. The Cholinergic neurons
1. The preganglionic fibers terminating in the adrenal
medulla, the autonomic ganglia (both parasympathetic
and sympathetic),
2. The postganglionic fibers of the parasympathetic
division use ACh as a neurotransmitter
3. The postganglionic sympathetic division of sweat
glands also uses acetylcholine.
4. In addition, cholinergic neurons innervate the muscles
of the somatic system and also play an important role
in the central nervous system (CNS).
29. Pharmacological actions of Ach:
Muscarinic actions:
1- CVS System:
Heart : M2 Receptor
⬇heart rate
⬇force of contraction
⬇conductivity
Blood Vessels : M3 Receptor
Vasodilation through the action on M3 Receptor that
activates nitric oxide ➡➡ that activates guanylate cyclase
➡the formation of cGMP
Blood Pressure:
⬇in the pressure due to bradycardia + Vasodilation
30. Pharmacological actions of Ach:
2. Gastrointestinal System:
Stimulation of tone & motility Stimulation of gastric enzymes
and acidity ( M1 Receptor ) and Relaxation of sphincters
3. Urinary System:
Relaxation of sphincter , Evacuation of the bladder
4. Bronchioles: Bronchoconstriction & ⬆secretions
5. Eye: Miosis due to the stimulation of ciliary muscle
contraction for the near vision and constriction of the pupille
sphincter muscle .
6. Exocrine glands: ⬆of secretions
N.B. These all muscarinic actions of Ach are blocked by
ATROPINE
31. Pharmacological actions of Ach:
Nicotinic actions:
1-Action on the autonomic ganglia ( Nn Receptor ) :
Ach Reversal in presence of atropine , high dose of Ach produce an
increase in the blood pressure due to :
stimulation of the sympathetic ganglia leading to release of
noradrenaline
stimulation of the adrenal medulla leading to the release of adrenaline &
noradrenaline
2- Action on the skeletal muscles ( Nm Receptor ) :
Leading to muscle twitches
The nicotinic actions of Ach are blocked by :
Ganglion blockers: hexamethonium
Neuromuscular blockers: d-tubocurarine
32. Adverse effect :
Flushing
GIT cramps
Bronchiole constriction ( asthma , dyspnea )
Sweating
Incresed saliva and other glands screations
Urinary urgency
May dcraese blood pressure and A - V block has be
reported in toxic doses.
36. Direct acting Cholinergic agonist
Acetylcholine
quaternary ammonium compound ,
cannot penetrate membrane,
Hydrolyzed by ACHE
Administration : Only IV administration
Receptor : both muscarinic and nicotinic activity
Action : 1- CVS : activates M3 receptors found blood vessels.
Bradycardia, ↓ cardiac out put, vasodilation and ↓blood pressure
2-GIT : increase secretion
3-eye : miosis
37. Direct acting Cholinergic agonist
Acetylcholine
4-genitourinary: urination
5-Bronchiolar : increase secretions --- Bronchospasm.
6- Secretory glands: stimulate secretion by
thermoregulatory sweat, lacrimal, and nasopharyngeal
glands
Therapeutic effect : No clinical use except to produce
miosis in ophthalmic surgery
38. Direct acting Cholinergic agonist
Bethanechol
Synthetic Choline Esters
cannot penetrate membrane
NOT Hydrolyzed by ACHE
Administration only for oral administration
Receptor : strong muscarinic activity , lacks nicotinic
actions
Action : directly stimulates muscarinic receptors
1-GIT: increase intestinal motility and tone.
2-genitourinary: stimulates the detrusor muscles of the
bladder whereas the sphincter is relaxed ---- urination
39. Direct acting Cholinergic agonist
Bethanechol
Therapeutic applications: Bethanechol used in
Paralytic ileus is given to activate M3 receptors to cause
gut motility especially after surgery. Postoperative
retention , Gastric atony .
Adverse effect : sweating, salivation, flushing, decreased
blood pressure, nausea, abdominal pain, diarrhea, and
Bronchospasm
40. Direct acting Cholinergic agonist
Carbachol
Synthetic Choline Esters
cannot penetrate membrane
NOT Hydrolyzed by ACHE
Administration : Locally instilled into eye
Receptor : both muscarinic and nicotinic activity
Action : effects on both CVS and GIT
• cause release of epinephrine from the adrenal medulla by
its nicotinic action ( first stimulate then depress )
• causing miosis and a spasm of ciliary muscle of the eye .
41. Direct acting Cholinergic agonist
Carbachol
Therapeutic applications: used as a miotic
agent to treat glaucoma by causing pupillary
contraction and ↓ intraocular pressure.
Adverse effect : little or no side effects occur due
to lack of systemic penetration (quaternary amine)
cant cross BBB
42. Direct acting Cholinergic agonist
Pilocarpine:
Alkaloid tertiary amine
Can penetrate the CNS
NOT Hydrolyzed by ACHE
receptor : exhibits muscarinic activity
Action :rapid miosis and contraction of the
ciliary muscle and spasm
- drop in intraocular pressure as a result of the
increased drainage of aqueous humor
- potent stimulators of secretions such as sweat,
tears, and saliva
43. Direct acting Cholinergic agonist
Pilocarpine:
Therapeutic applications: used primarily in
ophthalmology
drug of choice in treating glaucoma in both narrow-
angle and wide-angle . (Applied topically to the eye)
Sjögren syndrome" that characterized by dry mouth &
lack of tears, is treated with oral pilocarpine tablets
and cevimeline,
Adverse effects:
cause blurred vision, night blindness, and enter the brain
and cause CNS disturbances. It stimulates profuse
sweating and salivation
45. Indirect acting Cholinergic agonist:
Anticholinesterases :
Inhibitors of AChE (anticholinesterase agents or
cholinesterase inhibitors) indirectly provide a
cholinergic action by preventing the degradation
of ACh.
This results in an accumulation of ACh in the
synaptic space
This action could be reversible or irreversible
47. Indirect acting Cholinergic agonist:
Reversible anticholinesterases
1- Edrophonium :
• Short-acting drug from 10 to 20 minutes
• can be used in diagnosis of (Myasthenia gravis)
2- Physostigmine:
• medium-acting drug
• stimulate both M & N sites of the ANS
•⬆⬆intestinal & bladder motility
• antidote for (Atropine toxicity)
• can pass BBB so, it can CNS convulsions
• If level of Ach is increased , paralysis of skeletal muscles
can occur
48. Indirect acting Cholinergic agonist:
Reversible anticholinesterases
3- Neostigmine:
• medium-acting drug
• manage the symptoms of (Myasthenia gravis)
• antidote for competitive neuromuscular blockers
• can't pass BBB ,it cann’t cause the CNS convulsions
Contraindicated : intestinal and bladder obstruction .
4- Pyridostigmine & Ambenonium :
• medium-acting drug longer than Neostigmine
• Chronic management of (Myasthenia gravis)
Adverse effect :
Salivation , flushing ,
hypotension , nausea
, abdominal pain ,
diarrhea ,
bronchospasm
49. Indirect acting Cholinergic agonist:
Reversible anticholinesterases
Tacrine , Donepezil , Rivastigmine & galantamine :
They can pass BBB .SO, they are used Alzheimer disease
Tacrine cause hepatotoxicity
Major side effect is GIT distress
These drugs can be reversed by pralidoxime .
50. Indirect acting Cholinergic agonist:
IRReversible anticholinesterases
these drugs bind to the AchE and can't be reversed by
pralidoxime after aging with the enzyme
They are Organic phosphate esters :
1- Ecothiophate
2-Nerve gases ( sarin , tabun & soman )
3- Insectsides ( parathion )
• They produce intense miosis can be Used only in open
angle glaucoma
• Antidote; high dose of ATROPINE
51. Clinical picture of Organophosphorus
toxicity:
1.Muscarinic
Manifestations
2. Nicotinic
Manifestation
3. CNS manifestations:
(presence of these signs
varies with different
agents).
Restlessness, insomnia,
confusion & convulsions
52. Treatment of acute toxicity:
1- Endotracheal intubation:
a- Artificial respiration.
b- Aspiration of secretion.
2- Decontamination:
1. Remove contaminated clothes and wash the skin with NaHCO3 or
alcohol.
2. Stomach wash by NaHCO3 if ingested
3- Atropine:
Life saving : It Blocks peripheral muscarinic and CNS manifestations
I.V. 1-2 mg / 5 - 15 min. up to 25 – 50 mg / day till mydriasis, dry mouth, or
tachycardia.
Keep patient atropinized for at least 48 hours (0.4 mg/4 hours).
4- Cholinesterase reactivators (Oximes): early before aging
Pralidoxime (PAM): Does not pass BBB, regenerates Ch.E. at the N-M
junction. 1-2 gm I.V.
60. Antimuscarinic agents
A. Atropin
B. Scopolamine
C. Ipratropium and tiotropium
D. Tropicamide and cyclopentolate
E. Benztropine and trihexyphenidyl ,
Darifenacin, fesoterodine, oxybutynin,
solifenacin, tolterodine,and trospium
chloride
61. Antimuscarinic agents
Atropine
high affinity for muscarinic receptors.
It binds competitively and prevents ACh from binding
to those sites. Atropine acts both centrally and
peripherally.
Actions of Atropine:
a. Eye:
- mydriasis (dilation of the pupil),
- unresponsiveness to light,and cycloplegia (inability to
focus for near
vision).
b. Gastrointestinal (GI):
- antispasmodic to reduce activity of the GI tract.
Although gastric motility is reduced, hydrochloric acid
production is not significantly affected.
62. Antimuscarinic agents
Atropine
c. Cardiovascular:
- At low doses, a slight decrease in heart rate.
- Higher doses of atropine cause a progressive increase in
heart rate by
D. Secretions:
- dryness of the mouth (xerostomia).
The salivary glands are exquisitely sensitive to atropine. Sweat
and
lacrimal glands are similarly affected.
[Note: Inhibition of secretions by sweat glands can cause
elevated body temperature, which can be dangerous in
children and the elderly.]
63. Antimuscarinic agents
Atropine
Therapeutic uses of Atropine:
a. Ophthalmic:
Topical atropine exerts both mydriatic and cycloplegic Effects.
b. Antispasmodic: To relax the GI tract.
c. Cardiovascular: The drug is used to treat bradycardia.
d. Antisecretory:
To block secretions in the upper and lower respiratory tracts prior to
surgery.
e. Antidote for cholinergic agonists:
For the treatment of organophosphate (insecticides, nerve gases)
poisoning, of overdose of clinically used anticholinesterases such as
physostigmine, and in some types of mushroom poisoning (certain
mushrooms contain cholinergic substances that block
67. Ganglionic blockers
Ganglionic blockers specifically act on the nicotinic receptors of both
parasympathetic and sympathetic autonomic ganglia.
Nicotine :
Therapeutic uses of nicotine :
Smoking cessation
69. Neuromuscular blockers
These drugs block cholinergic transmission between motor nerve
endings and the nicotinic receptors on the skeletal muscle.
They possess some chemical similarities to ACh, and they act either
as antagonists (no depolarizing type) or as agonists (depolarizing
type) at the receptors on the endplate of the NMJ.
Neuromuscular blockers are clinically useful during surgery to
facilitate tracheal intubation and provide complete muscle relaxation
at lower anesthetic doses, allowing for more rapid recovery from
anesthesia and reducing postoperative respiratory depression.
70. Neuromuscular blockers
Nondepolarizing (competitive)
blockers:
The neuromuscular-blocking agents have significantly increased the
safety of anesthesia, because less anesthetic is required to produce
muscle relaxation, allowing patients to recover quickly and completely
after surgery.
Neuromuscular blockers should not be used to substitute for
inadequate depth of anesthesia.
71. Mechanism of action:
At low doses:
Nondepolarizing agents competitively block ACh at the nicotinic
receptors. Thus, these drugs prevent depolarization of the muscle
cell membrane and inhibit muscular contraction.
Their competitive action can be overcome by administration of
cholinesterase inhibitors, such as neostigmine and edrophonium,
which increase the concentration of ACh in the neuromuscular
junction.
At high doses:
Nondepolarizing agents can block the ion channels of the motor
endplate. This leads to further weakening of neuromuscular
transmission, thereby reducing the ability of cholinesterase
inhibitors to reverse the actions of the nondepolarizing blockers.
With complete blockade, the muscle does not respond to direct
electrical stimulation.
72. Neuromuscular blockers
Depolarizing blockers:
Depolarizing blocking agents work by depolarizing the plasma
membrane of the muscle fiber, similar to the action of ACh.
However, these agents are more resistant to degradation by
acetylcholinesterase (AChE) and can thus more persistently
depolarize the muscle fibers.
Succinylcholine is the only depolarizing muscle relaxant in use
today.
75. Adrenergic agonist
The adrenergic drugs are affect the adrenoceptors ( Alfa and Beta ) which is
stimulated by neurotransmitter norepinephrine or epinephrine.
Norepinephrine is the primary neurotransmitter .
Drugs activating (adrenoceptor) sympathomimetics drugs .
Sympathomimetics drugs that activate the adrenoceptors Dirctly ( direct acting
agonist ) or Indirectly by enhancing release or blocking reuptake of
norepinephrine ( indirect acting agonist )
82. Adrenergic receptors
For the α receptor, the rank order of potency is epinephrine >
nor epinephrine > isoproterenol
For the β receptor , the rank order of potency is isoproterenol
>epinephrine > nor epinephrine
84. Characteristics of adrenergic
agonist
The adrenergic drugs are derivatives of β-phenylethylamine.
Substitutions on the benzene ring or on the ethylamine side chains
produce abilities to differentiate between α and β receptors and to
penetrate the CNS.
Two important structural features of these drugs are
The number and location of OH substitutions on the benzene ring
( metabolized by COMT )
The nature of the substituent on the amino nitrogen
(oxidized by monoamino oxidase MAO )
104. Adrenergic antagonist
The adrenergic antagonist drugs are inhibit
or block the adrenoceptors ( Alfa and Beta )
Drugs blocking (adrenoceptor)
sympatholytics drugs .
The adrenergic antagonists act by either
reversibly or irreversibly attaching to the
adrenoceptors, thus preventing activation by
endogenous catecholamines.
It can be classified according to their activity
on
α or β receptors & the effect of
neurotransmitter uptake or release.
107. α-ADRENERGIC BLOCKING
AGENTS
α-Adrenergic blockers block α adrenoceptor affect blood pressure –
> ↓ peripheral vascular resistance ---> reflex tachycardia resulted
from the lowered blood pressure.
All α-Adrenergic blockers revers the α agonist actions of
epinephrine.
108. α-ADRENERGIC BLOCKING
AGENTS
Non selective
Phentolamine
Phenoxybenzamine
Drug
reversible and competitive Block both α1
and α2 receptors
short duration of action
irreversible and non competitive
Block both α1 and α2 receptors
Long duration of action
Recept
or
1- Block α1 receptor : prevent vasoconstriction --- decreases PR --- reduce BP ---baroreceptor
reflex --- tachycardia
2- Block presynaptic inhibitory α2 enhanced release of NE --- stimulate β1 in heart --- increase
CO
3- Epinephrine reversal : the vasoconstrictive action of epinephrine is interrupted, but
vasodilation of other vascular by stimulation of β2 receptors is not blocked. in the presence of
α blockers epinephrine reduce BP
action
Pheochromocytoma
Rarely used for the treatment of
impotence.
Pheochromocytoma
Raynaud's disease
Autonomic hyperflexia
Therap
eutic
effect
Arrhythmias and anginal pain
Postural hypotension, nasal
stuffiness, nausea, and vomiting.
Side
effect
109. α-ADRENERGIC BLOCKING
AGENTS
Selective
Yohimbine
Prazosin, terazosin, doxazosin, alfuzosin, and
tamsulosin
Drug
selective competitive α2 blockers
Selective competitive α1 blockers
Receptor
promotes norepinephrine release
through blockade of α2 receptors in both
the central nervous system and the
periphery. reverses the antihypertensive
effects of α2 adrenoceptor agonists such
as clonidine
Hypotension --- decrease peripheral vascular
resistance and lower arterial blood pressure by
causing the relaxation of both arterial and venous
smooth muscle
Action
Male erectile dysfunction Orthostatic
hypotension
Used to relieve vasoconstriction
associated with Raynaud's disease
Hypertension --- Prazosin, terazosin, doxazosin
benign prostatic hypertrophy --- alfuzosin
CHF --- congestive heart failure
Therapeu
tic effect
is contraindicated in CNS and
cardiovascular conditions because it is a
CNS and cardiovascular stimulant.
First dose : orthostatic hypotensive dizziness, a lack of
energy, nasal and congestion, headache, drowsiness,
orthostatic hypotension. inhibition of ejaculation
Side
effect
112. β- Adrenergic
Blocking Agent
β-blockers divided to nonselective (β1
and β2 receptors), selective (β1
receptors) & α and β adrenoceptors
antagonists.
All β-blockers lower blood pressure, they
do not induce postural hypotension,
because the α adrenoceptors remain
functional.
β-Blockers are effective in treating
hypertension, angina, cardiac
arrhythmias, myocardial infarction, heart
failure, hyperthyroidism, and glaucoma.
113. Classification of β- Adrenergic Blocking
Agent
Non selective (β1
and β2 receptors)
Selective (β1 receptors)
α and β
adrenoceptors
antagonists
Propranolol Nadolol
&Timolol
Acebutolol
Atenolol
Bisoprolol
Esmolol
Metoprolol
Nebivolol
Labetalol Carvedilol
115. Propranolol
Therapeutic uses:
Hypertension : Decreased cardiac output is the primary mechanism, but
inhibition of renin release from the kidney, decrease in total peripheral
resistance with long- term use, and decreased sympathetic outflow from the
CNS also contribute to the antihypertensive effects.
Angina pectoris : Decreases the oxygen requirement of heart muscle →
effective in reducing chest pain)
Myocardial infarction : By blocking of the actions of circulating
catecholamines, which would increase the oxygen demand in an already
ischemic heart muscle.
Migraine: Due to its lipophilic nature that allows it to penetrate the CNS, it
reduces migraine episode
Hyperthyroidism : It is effective in blunting the widesprea
d sympathetic stimulation during hyperthyroidism.
116. Propranolol
Pharmacokinetics:
Propranolol is almost completely absorbed, and only about 25% of an
administered dose reaches the circulation because of first pass
metabolism.
The volume of distribution of propranolol is quite large (4 L/kg), and the
drug readily crosses the blood–brain barrier due to its high lipophilicity.
Propranolol is extensively metabolized, and most metabolites are
excreted in the urine
117. Propranolol
Adverse effects:
Bronchoconstriction: due to blockade of β2
receptors.
Arrhythmias : never be stopped
abruptly because of the risk of precipitating cardiac
arrhythmias, it must be tapered off gradually over a period
of at least a few weeks.
Sexual impairment
Metabolic disturbances: Blockade leads to
decreased glycogenolysis and decreased glucagon
secretion. It also hides he symptoms of
hypoglycemia. In addition to its effect of serum lipid
profile.
CNS effect: Depression, dizziness, weakness,
visual disturbances, short- term memory loss.
118. Propranolol
Drug interactions:
Drugs that interfere with, or inhibit, the metabolism
ofpropranolol, such as cimetidine, fluoxetine, paroxetine, and ritonavir,
may potentiate its antihypertensiveeffects. Conversely, those
that stimulate or induce its metabolism, such as barbiturates,
phenytoin, and rifampin, can decrease the effect .
119. Nadolol and timolol:
Nadolol and Timolol are more potent than propranolol
Nadolol has a very long duration of action.
Timolol reduces the production of aqueous humor in the eye. It
is used topically in the treatment of chronic open-angle glaucoma
and for systemic treatment of hypertension
Timolol, betaxolol, or carteolol, are effective in diminishing
intraocular pressure in glaucoma. When administered
intraocularly, the onset about 30 minutes, and the effects last for
12 or 24 hours.
121. Acebutolol, Atenolol, Betaxolol, Bisoprolol,
Esmolol, Metoprolol,And Nebivolol
β1 receptors antagonists minimize the unwanted
bronchoconstriction (β2 effect) seen with propranolol use in
asthma patients.
This cardioselectivity is most pronounced at low doses and is
lost at high doses.
Actions and therapeutic use:
In hypertensive patients with impaired pulmonary function, can
be used to lower blood pressure. Esmolol is only available IV and
has a very short half-life.
For chronic stable angina, it considered as first-line therapy with
increasing exercise tolerance.
Bisoprolol and the extended-release formulation of metoprolol are
indicated for the management of chronic heart failure.
Nebivolol releases nitric oxide from endothelial cells and causes
vasodilation.
122. Acebutolol and Pindolol: Antagonists with
partial agonist activity
These drugs also have the ability to weakly stimulate both β1
and β2 receptors and are said to have intrinsic
sympathomimetic activity (ISA).
The result of these opposing actions is a diminished effect on
cardiac rate and cardiac output.
β-blockers with ISA minimize the disturbances of lipid and
carbohydrate metabolism that are seen with other β-blockers.
It is effective in hypertensive patients with moderate
bradycardia but not used for stable angina or arrhythmias due
to their partial agonist effect
125. Reserpine
It blocks the Mg2+/adenosine triphosphate–dependent
transport of biogenic amines (norepinephrine, dopamine,
and serotonin) from the cytoplasm into storage vesicles in
the adrenergic nerve terminals → Depletion of biogenic
amines.
It has been used in management of hypertension but has
largely been replaced with newer agents with better side
effects profiles and fewer drug interactions.
