This document provides information on neurons and the nervous system. It discusses: 1) The three main types of neurons - afferent, efferent, and interneurons. It describes their functions in signal transmission. 2) The parts of neurons - cell body, dendrites, axons. It explains how axons conduct action potentials to different parts of the body. 3) How action potentials are initiated when the membrane potential reaches threshold. The influx of sodium ions causes rapid depolarization, and then repolarization occurs as potassium ions efflux. 4) Synaptic transmission and how calcium influx causes neurotransmitter release by exocytosis at the synaptic knob to continue the signaling process between neurons.

1. Brian Tuschl, Pharm D.

2. 


Neurons - are a communication center.
Afferent transmission, sensory neurons, impulses
toward the spinal cord & brain
Efferent transmission, motor neurons, impulses
away from the spinal cord, brain & glandular tissue
Multipolar – one axon with several dendrites
 Bipolar – one axon and one dendrite
 Unipolar – one axon and NO dendrites

Axons are an extension of the neuron. they conduct the
transmission of information, afferently or efferently, to
different parts of the body through the use of AP’s.

3. 
Neuron – Neurons conduct impulses through
action potentials (AP). Neurons have a cell body
which contain free & fixed ribosomes, Golgi body
apparatus & mitochondria which produces ATP for
energy. All of these work in conjunction with each
other for the ultimate release of sodium. Once an
action potential begins and sodium is released it
travels down the axon to the ultimately reach the
synaptic knob where it there interacts with calcium
to release the many NT’s or catecholamines that are
stored and are then released into the synapse.

4. 
AP’s are created currents, by reaching threshold, that
are propagated at the initial segment of the axon that
extends the length of the axon & ends at the synaptic
knob. This ultimately causes a large influx of Ca++
which forces the release of NT or catecholamines
(ACh, Epi, NE & Dopamine) stored in vesicles at the
synaptic knob. This Ca++ dependent process that
releases NT’s out of its vesicle and into the synapse
to continue the communication process is called
“exocytosis.” These NT’s and Catecholamines are
used for our senses; such as touch (feeling), motor
(movement) they also affect mood, fight or flight

5. 
AP’s are an “all or none” process. AP’s are initiated
when a threshold of at least -60 mV to -55 mV is
reached. This stimulus is large enough to open the
voltage gated Na+ channel. “A graded depolarization
is like the pressure on the trigger of a gun and the
AP is the firing of the gun.” With no or not enough
stimulus there is no AP & the transmembrane
potential returns to resting levels. The strength of the
AP are independent of the depolarizing stimulus as
long as the gradient is strong enough to reach
threshold.

6. 



1) Depolarization to threshold “All or None”
2) Opening voltage regulated Na+ channels. Upon
depolarization Na+ chan. open. Now more positive ions enter
the cytoplasm which cause a shift from a neg. potential at
resting state to a positive one upon depolarization.
3) Na+ chan. Inactivation & K+ chan. Activation. As the
positive potential reaches +30mV the Na+ gates begin to close
& K+ begins moving out of the cytoplasm shifting the potential
back to a negative resting state & repolarization begins.
4) The return to normal permeability. As the membrane
potential reaches -60mV the Na+ channel become capable of
opening again for depolarization. As the K+ channel begin
closing as the potential reaches -60mV. The K+ continues to
rush out & the potential can reach -90mV causing
hyperpolarization. The potential returns to -60mV (resting
state) & the AP is over.

7. 

Synaptic Transmission – drugs can affect the firing rate, the
release of NT or catecholamines or the crossing of
neurotransmitters or catecholamines across the synaptic cleft.
If the cell did not have a receptor site the NT or
catecholamines could/would not affect the cell so no
activation would occur.
Many drug interactions occur b/c of drugs competing for the
same rec site.

9. 







1) Skeletal muscle
2) Cardiac output
3) Vascular tone
4) Respiration
5) GI function
6) Uterine motility
7) Glandular secretions
Also effects pain perception, ideation and
mood

10. Increase ↑
Constriction
Increase ↑
Decrease ↓
Constipation
Decrease ↓
Xerostomia
Mitosis (Mydriasis)
Ejaculation
Relaxation
Contraction
Cardiac Output/Heart Rate
Vascular Tone
Respiration
GI
GI
GI Secretions
Secretions
Eye
Sex
Uterine SM
Prostate
Decrease ↓
Dilate
Decrease ↓
Increase ↑
Diarrhea
Increase ↑
Salivation
Miosis
Erection

11. 







Agonist – directly activate receptor (morphine,
epi, insulin)
Antagonist – prevent receptor activation
(naloxone, antihistamines, beta blockers)
Direct acting – Stimulate receptor
Indirect acting – Stimulate release of NT
Sympathomimetic – adrenergic (SNS)
Sympatholytic – antiadrenergic
Parasympathomimetic – Cholinergic (PSNS)
Parasympatholytics – anticholinergic

14. 1)
2)
3)
4)
5)
All PREganglionic neurons of the PSNS & SNS release ACh
as their neurotransmitter.
All postganglionic neurons of the PSNS release ACh as the
neurotransmitter. – all the way to muscarinic receptor
Most postganglionic neurons of the SNS release NE as their
neurotransmitter. – acts on beta 1 and alpha 1
Epi is the main NT released by the adrenal medulla (which is
ONLY a feature of the SNS and is considered prejunctional)
All motor neurons to the skeletal muscles directly release
ACh as their neurotransmitter. – somatic nervous system
1)
Parkinson’s disease pts. Dopamine misbehaves, ACh levels increased 
tremors. THEREFORE give dopamine agonists to lower ACh levels.

15. 1)
Epinephrine - released ONLY by adrenal medulla which also
releases NE (unlike Epi, NE is also released by neurons). Epi is also the
only NT that activates all adrenergic rec (alpha 1 & 2 & beta 1 & 2).
2)

3)
Norepinephrine – released by postganglionic neurons of the SNS,
except sweat glands (which releases ACh at muscarinic rec at the target
organ in the SNS) NE activate adrenergic rec alpha 1 & 2 and beta 1
NOT beta 2 or dopamine rec.
NE is not broken down in the synapse but is taken back up through the
nerve terminal (alpha 2) to be broken down and restored by monoamine
oxidase (MAO.)
Dopamine - precursor to NE and epi.
Can activate alpha 1, beta 1 and dopamine receptors.
1)
Acetylcholine – is the only preganglionic (prejunctional,
preneuronal) NT of both the PSNS & the SNS. Postganglionically it is the
NT for the PSNS that activates muscarinic and nicotinic M rec. ACh also
activates the sweat glands muscarinic rec in the SNS.

16. 









1) ACh
Activate cholinergic receptors (muscarinic, nicotinic
receptors “m” and “n”)
Is broken down by acetyl cholinesterase (AChE)
2) Epi
Can activate alpha and beta receptors but NOT dopamine
receptors.
Only NT that acts on beta 2 receptors
Released from adrenal medulla NOT from neuron nerve
terminal
Dilates blood vessels (lungs, heart & skeletal muscle) Epi
counteracts anaphylactic shock
Increase glycogenolysis (glycogen to glucose)
Relax uterine smooth muscle

17. PNS regulates, depending on stimulus & the target
organ (cholinergic or anticholinergic), an increased or
decreased effect on these organs
PNS Receptor Activation(NicotinicN rec. activation)

Neurotransmitter is ACh.

NT on all of the ANS ganglia (pre & post) & the adrenal
medulla

Stimulation of parasympathetic & sympathetic
POSTganglionic nerves release epi from the adrenal
medulla

PNS Receptor Activation (NicotinicM rec. activation)

Neurotransmitter is ACh.

NT ACh goes straight to the neuromuscular junction

18. PNS Receptor Activation (Muscarinic rec activation)
 1)Eye - Contraction of ciliary muscle for near vision & Miosis (dec
pupil diameter) – pinpoint pupils




2) Heart – Dec heart rate, hypOtension
3) Blood Vessels – Vasodilation (lower BP!)
4) Lung – Contraction of bronchi (difficulty breathing)
5) Bladder - Contraction of detrusor & relaxation of trigone & sphincter
muscle (causes urination) (increased urination!!!)

6) GI Tract - Salivation, inc gastric secretions & intestinal tone &
motility, defecation

6) Sweat glands - sweating is a SNS response but is through activation
of muscarinic rec by ACh

7) Sex organs – Erection (due to dilation of blood vessels) this is only
spot where the SNS and PSNS work together (PSNS/erection &
SNS/ejaculation)

19. 





Selectively block ACh at muscarinic receptor site
Increased heart rate
Decreased salivation, bronchial dilation, sweat
glands, acid secretion
Smooth muscle relaxation of bronchi,
decreased GI and bladder motility
Mydriasis (dilation) focus lens for far vision
NOT all muscarinic receptors have the same
sensitivity. Clinical significance is dose
dependent.

20. 





Xerostomia (Dry mouth)
Blurred vision and photophobia
Elevation of intraocular pressure
Constipation
Anhidrosis (deficiency of sweat)
Tachycardia

21. Drugs function in the PSNS:
Notice that the conditions of the PSNS (or drugs that
stimulate PSNS conditions) are functions that would
normally happen in a resting state NOT in a “fight or
flight” condition
 1) Slowing of the heart
 2) Increased gastric secretion
 3) Emptying of the bladder
 4) Emptying of the bowel
 5) Focusing the eye for near vision
 6) Constricting the pupil
 7) Contracting bronchial smooth muscle

22. 

3 main functions:
1) Regulating the CV system



2) Regulating body temperature




Increased cardiac output
Cause vasoconstriction – increases BP
Regulate blood flow to skin
Promote secretion of sweat to keep body cool
Erection of hair
3) Implementing the “fight or flight” reaction





Increased heart rate & blood pressure
Shunt blood away from skin to skeletal muscle (clammy)
Dilate bronchi for more oxygen (deeper breaths)
Dilate pupils for increased vision
Provide glucose for brain, fatty acids for muscles for inc energy

23. PNS Receptor Activation
(Alpha 1 & 2 and Beta 1 & 2 receptor activation)
(Adrenergic)
Alpha 1
Eye
Arterioles
Veins
Sex organ
Prostate
Bladder
1) Contraction of radial & sphincter muscle & inc. pupil size
2) Constriction of arterioles (skin, viscera mucous membrane)
3) Venous constriction
4) Male ejaculation
5) Contraction of prostate
6) Contraction of trigone & sphincter muscle in bladder
Alpha 2
Presynaptic nerve terminals 1) Inhibition of transmitter release

24. PNS Receptor Activation (Alpha 1 & 2 and Beta 1 & 2
rec activation) (Adrenergic)
Beta 1
Heart 1) Inc HR, force of contraction, AV conduction velocity
Kidney 2) Renin release
Beta 2
Arterioles 1) Dilation of arterioles in heart, lung & skeletal muscle
Lungs
Uterus
Liver
Skeletal
muscle
2) Dilation of the bronchi in the lungs
3) Relaxation of the uterus
4) Glycogenolysis in the liver
5) Enhanced contraction of skeletal muscle & glycogenolysis
Dopamine
Kidney 1) Dilation of kidney vasculature (used for shock)

25. 4) Beta 2
Bronchial dilation
 Relaxation of uterine smooth muscle
(Terbutaline – Beta 2 adrenergic agonist) stops premature
pregnancy contractions
 Dilation of lungs and arterioles, heart contractility, skeletal
muscle contraction and glycogenolysis
 Liver – Glycogenolysis
5) Dopamine
 Is considered adrenergic but does not respond to epi and
NE and is primarily found in the CNS.
 Receptor located in the vasculature of the kidney. When
activated causes dilation and enhances renal perfusion
 Used for shock and hypotension.


26. NT RECEPTOR ACTIVATION
1.
2.
3.
Epi
NE
Dopamine
RECEPTOR ACTIVATION EFFECT
1.
2.
3.
4.
Alpha1 Activation Drugs
1.
2.
3.
4.
5.
Epi
NE
Dopamine
Phenylephrine
Ephedrine
1.
1.
2.
Mydriasis (pupil dilation)
Vasoconstriction
Ejaculation
Bladder Contraction
 Trigone & Sphincter
Bladder Dilation
 Detrusor
Piloerection (Goosebumps)
Prostrate Muscle
Contraction

27. NT RECEPTOR ACTIVATION
1.
2.
Epi
NE
Alpha2 Activation Drugs
1. Epi
2. NE
3. Ephedrine
RECEPTOR ACTIVATION EFFECT


Located on nerve terminal
NOT on organ tissue & are
referred to as Presynaptic or
Prejunctional
Regulates transmitter release

28. NT RECEPTOR ACTIVATION
1.
2.
3.
Epi
NE
Dopamine
RECEPTOR ACTIVATION EFFECT
1.
Beta1 Activation Drugs
1.
2.
3.
4.
5.
6.
Epi
NE
Isoproterenol
Dopamine
Dobutamine
Ephedrine
1.
Heart
•
Increased Heart rate
•
Increased Force of
contraction
•
Increased Velocity of
impulse thru AV node
Kidney
•
Activation of renin

29. NT RECEPTOR ACTIVATION
1.
Epi
RECEPTOR ACTIVATION EFFECT
1.
2.
Beta2 Activation Drugs
1. Epi
2. Isoproterenol
3. Terbutaline
1.
2.
3.
4.
Bronchial dilation
Relaxation of uterine smooth
muscle
 Terbutaline (β2 adrenergic
agonist)
Stops premature
pregnancy contractions
Dilation of arterioles
Heart contractility
Skeletal muscle contraction
Liver (glycogenolysis)

30. 





1) Muscarinic agonist (mimic ACh) Bethanechol
2) Muscarinic antagonist (block ACh) Atropine
3) Ganglionic stimulating (blocks ACh at
nicotinicn rec. in large doses, reverse in small
doses) nicotine
4) Ganglionic blocking agents (mecamylamine)
5) Neuromuscular blocking agents (blocks ACh
at nicotinicm rec.) d-Tubocurarine, succinylcholine
6) Cholinesterase inhibitors (prevent breakdown
of ACh and ACh inhibitors) neostigmine,
physostigmine

31. Category
Agents
Endogenous
dopamine
[Inotropin]
norepinephrine
[Levophed]
epinephrine
[Adrenalin]
Synthetic
dobutamine
[Dobutrex]
isoproterenol
[Isuprel]
phenylephrine
[Neo-Synephrine]

32. 
Catecholamines :

(epi, NE, dopamine, dobutamine, isoproterenol)
 Short duration of action
 Cannot give by mouth (PO)
 Do not cross blood-brain barrier (bbb)
Noncatecholamines:
(Phenylephrine, ephedrine, terbutaline)
 Longer duration of action
 Can give PO
 Crosses bbb


33. 

McHenry (2006), pg 425
Direct Acting

34. Direct Acting
Indirect-Acting
acetylcholine
ambenonium
echothiophate
edrophonium
bethanechol
demecarium
isoflurophate
neostigmine
carbachol
physostigmine
pyridostigmine
methacholine
pilocarpine

35. salivation
lacrimation
urinary incontinence
diarrhea
gastrointestinal cramps
emesis
at recommended doses the cholinergics primarily affect
{M} but at high doses {N}

36. 
MOA:






Stimulates cholinergic rec. in the smooth muscle of the urinary
bladder & GI tract resulting in
1) Increased peristalsis
2) Increased ureteral peristaltic waves
3) Increased GI & pancreatic secretions
4) Bladder muscle contraction
Pharmacotherapeutics:
– urinary
retention, loss of tone in GI tract
– unlabeled use: GERD (has little effect on nicotinic or
skeletal muscles)

37. 
Pharmacokinetics and dose:
–
–
–
–
–

Pharmacodynamics:


PO; 10-50 mg tid or qid (5-10 mg at hourly
intervals until desired response)
Give on an empty stomach
SC ; 2.5-5 mg tid or qid
NEVER IM OR IV
rapid onset – 30-90 minutes/duration up to 6/hours
Same effects as acetylcholine
Overdose

Atropine I.V. 0.6 mg every 2 hours per clinical
response

38. Adverse Reactions:






GI – Abdominal cramps, diarrhea, N/V, salivation
Genitourinary – Urinary urgency
Ocular – Lacrimation, miosis
Bronchial constriction/asthma attacks
CV - Hypotension/tachycardia/flushed skin
Sweating

39. Contraindications:



Mechanical obstruction of GU or GI tract
Peritonitis
Parkinson's disease







Low Dopamine levels = high ACh already!!! Bethanechol
acts just like ACh which pushes it higher!
Hypotension / hypertension
Bradycardia
Epilepsy
Asthma
Hyperthyroidism
Pregnancy (cat. C)

40. Drug Interactions:

Cholinesterase inhibitors - > cholinergic





ACh + Bethanechol = TOO MUCH
Ganglionic blockers - severe hypotension
Quinidine - antagonize cholinergic
Pilocarpine - > cholinergic effect
Carbachol - > cholinergic effect

41. Natural
Synthetic
atropine
clidinium
dicyclomine
glycophyrrolate
belladonna
hexocyclium
homatropine
isopropamide
mepenzolate
methantheline
hyscocyamine methscopolamine
scopolamine
oxyphencyclamine propantheline
tridihexethyl

42. Body
System
CNS
Cholinergic Blocker Effects
decreases muscle rigidity & tremors
high doses: drowsiness, disorientation, &
hallucinations
Eye
dilates pupils [mydriasis]
accommodation: paralyzes ciliary muscles
[cycloplegia]
CV
small doses: decrease heart rate
large doses: increase heart rate

43. Body
System
RESP
GI
GU
Glandular
Cholinergic Blocker Effects
decrease bronchial secretions
dilate bronchial airways
relaxes smooth muscle tone of GIT
decreases intestinal & gastric secretions
decreases GI motility & peristalsis
relaxes detrusor muscle of bladder
increases constriction of internal
sphincter
these two may result in urinary retention
decreases bronchial secretions,
salivation, & sweating

44. 




Completely block ACh at the receptor site
Atropine (belladonna alkaloid)
Found naturally in Atropa belladonna (deadly
nightshade) and Datura stramonium (jimson
weed, stinkweed)
At high doses effect nicotinic receptors also.
Exerts effect on: heart, exocrine glands, smooth
muscles and eye

45. Dose
Low dose
High dose
Response produced
Salivary gland (decreased secretion)
Sweat glands (decreased secretion)
Bronchial glands (decreased secretion)
Heart (increased rate)
Eye (Mydriasis, blurred vision)
Urinary tract (interference w/ voiding)
Intestine (decreased tone and motility)
Lung (dilation of bronchi)
Stomach (decreased acid secretion)

46. MOA:

Blocks the action of ACh at parasympathetic receptor
sites in smooth muscle, secretory glands and the CNS
results in
1) Increased cardiac output
2) Dries secretions
3) Antagonizes histamine and serotonin

47. Pharmacotherapeutics:
PO, SQ, IM, IV, Aerosol, endotracheal instillation
Injection
1) Preoperative to inhibit salivation & secretions
2) Tx of symptomatic sinus bradycardia, AV block (nodal
level), ventricular asystole,
3) Antidote for organophosphate pesticide poisoning
Ophthalmic
1) Produce mydriasis & cycloplegia for examination of the
retina and optic disc.
PO
1) Inhibit salivation and secretions

48. 
Pharmacokinetics:









Easily absorbed and widely distributed
Crosses blood-brain, placental barrier and trace amounts
enter breast milk
Hepatic metabolism
Excreted in the urine
IV rapid onset
IM onset 5-50 min
PO onset 1-2 hours
Half life 2-3 hours
Dose >5kg 0.01-0.02 mg/kg/dose to a max 0.4 mg/dose
30 to 60 minutes preop.

49. 



Adverse Effects:
Dose related and vary greatly and are 1) limited 2)
Significant 3) Life-threatening
Limited/Common: dry mouth, blurred vision, urinary
hesitancy, constipation, palpitations, anhidrosis
Significant: tachycardia, photophobia, confusion,
insomnia, delirium, hallucinations, rash, allergic reaction,
impotence, suppression of lactation, muscular
incoordination, hypertension, vomiting, bloating, paralytic
ileus, etc.

50. Atropine Intoxication:






Extreme dry mouth, dry upper respiratory tract, dry skin
("dry as a bone") foul breath
Diminished visual acuity due to pupil dilation ("blind as a
bat")
Elevation of body temperature ("hot as a furnace") hot ,
dry flushed skin
Hallucinations, bizarre behavior, confusion, delirium, <
memory ("mad as a hatter")
Overdose:
Physostigmine (AChE inhibitor) 0.5 mg or 0.02 mg/kg in
children. SQ or slow IV

51. Contraindications:









Narrow-angle glaucoma
CAD
Urinary/GI obstruction
Paralytic ileus
Ulcerative colitis
Hiatal hernia
Hepatic/renal disease
Lung disease/asthma
Caution


adults over 40
older adults

52. Drug Interactions:
Increased Effect/Toxicity of Atropine
 Antihistamines, phenothiazines, TCA’s and
other drugs with anticholinergic activity.
Decreased Effect/Toxicity of Atropine
 Metoclopramide, cisapride, bethanechol
Drugs with cholinergic mechanisms

53. Nursing management:
Monitor VS frequently
Assess bowel sounds, frequency of bowel
movements, voiding patterns
Side effects of other drugs
Frequent fluids, ice chips, hard candy
Frequent sponge baths
Assess lung sounds
Have suction equipment available
Elevate side rails
Report changes in LOC

54. MOA:
 Low doses activate nicotinic receptors
 High doses block nicotinic receptors
 Activates receptors in the CNS which makes it
highly addictive.
 Activates receptors in the autonomic ganglia to
release NE and release of epi from the adrenal
medulla
 At doses of smoking it has no effect on skeletal
muscle nicotinic receptors

55. Pharmacokinetics:
 Widely distributed
 90-98% of nicotine that enters the lungs enters
the blood stream
 Nicotine crosses placenta
 Reaches breast milk and can be toxic
 Half life 1-2 hours
 Excreted by the kidneys

56. Pharmacotherapeutics :(Low dose effects)

Cardiovascular
Releases NE from sympathetic nerves and NE and epi from
the adrenals causing blood vessel constriction, accelerate
the heart, ventricular contraction which causes increase
blood pressure
GI
 By activation of nicotinic rec. in the parasympathetic
system inc. GI motility and secretions.


CNS
Stimulates respiration, inc. alertness, cognition and
memory and by activating dopamine activates pleasure
center.

57. Acute poisoning :(40 mg and up)
 High doses block nicotinic receptors
Sx include CNS, GI and CV
 N/V, diarrhea, cold sweat, confusion, fainting, pulse
is rapid, weak and irregular
 Death by respiratory paralysis

Antidote:
No real antidote. Give activated charcoal recovery in
hours

58. 2 types:
1) Reversible inhibitors
2) Irreversible inhibitors

Reversible:

1) Neostigmine (Prostigmin) PO, IV, IM, SQ

2) Ambenonium (Mytelase) PO

3) Pyridostigmine (Mestinon) PO, IV

4) Edrophonium (Tensilon, Reversol) IM, IV

5) Physostigmine (Antilirium) IM, IV

6) Donepezil (Aricept) PO

7) Galantamine (Reminyl) PO

8) Rivastigmine (Exelon) PO

9) Tacrine (Cognex) PO

Irreversible:
1) Echothiophate (Phospholine Iodide) topical

59. MOA:
 Prevents the breakdown of ACh into choline
and acetic acid(indirect-acting cholinergic
agonist)
 Has no specificity so it has a broad spectrum
response
 Same effect and adverse effects as those of
direct-acting muscarinic agonist
 Mostly used in Myasthenia Gravis

60. Pharmacokinetics:

Carries Nitrogen with 4 bonds which has a
positive charge so does not cross membranes easily
(GI, bbb, placenta)

Physostigmine – only 3 bonds so no positive
charges so crosses membranes much easier

Once bound to AChE it remains in place for a long
time.

PO, IV, IM, SQ

DOA – 2-4 hours
Overdose:
Atropine

62. Adrenalin, Bronkaid Mist, Primatene Mist, Epifrin
MOA :

Stimulates Alpha 1 & 2 and Beta 1 & 2
 Relaxation of smooth muscle in the bronchial tree
 Cardiac stimulation
 Dilation of skeletal muscle
 Direct acting, nonselective
Pharmacokinetics:





Crosses placenta
IV, SQ, Intratracheal, , Intracardiac injection, IM, Nebulizer, intranasal
Metabolism – MAO & COMT & circulating hepatic metabolism
Excretion – Urine
Short half life

63. Pharmacotherapeutics:
 Anaphylactic shock
 Bronchoconstriction
 Cardiac arrest
 Overcome AV heart block
 Elevate blood pressure
 Control superficial bleeding
 Delay absorption of local anesthetics

64. Adverse Effects:
 CV – Tachycardia, HTN, chest pain, vasoconstriction,
arrhythmia, sudden death





CNS – Nervousness, HA, anxiety, insomnia
GI – Xerostomia, N/V
Genitourinary – Urinary retention
Respiratory – Wheezing, dyspnea
Necrosis - b/c of vasoconstriction minimized by
phentolamine (alpha-adrenergic antagonist)

Hyperglycemia – b/c breakdown of glycogen
through activation of beta2 receptors in liver & skeletal
muscle (be careful for diabetics!!)

65. Drug Interactions:
 MAO inhibitors – prolongs and intensifies effects
 TCA’s – Block re-uptake and prolongs effect
 General Anesthetics
 Alpha-Adrenergic blockers – block receptor activation
 Beta-Blockers – block effects

66. 

Presynaptic alpha2 activation in the ANS has
little clinical relevance but has significant
relevance in the CNS.
Activation inhibits NE release

67. Therapeutic use of Alpha1 activation:
Vasoconstriction (blood vessels on skin, viscera of mucus
membrane)

1) epi used to stop topical bleeding (used in boxing)

2) Nasal congestion (nasal phenylepherine, ephedrine
orally)
3) used during anesthesia slows absorption of
anesthetic

4) Hypotensive pts.
Mydriasis
Adverse Effects of Alpha1 Activation:
1) HTN
2) Necrosis
3) Bradycardia reflex

68. All relevant response to beta1 is in the heart
Therapeutic Applications:
1) Cardiac arrest – beta1 activation inc. contraction if heart
is not beating.
2) Heart failure – beta1 activation cause positive inotropic
effect (inc. force of contraction)
3) Shock – inc. force of contraction and heart rate
4) AV block – Enhances impulse conduction through the
AV node.
Adverse Effects:
1) Altered heart rate/rhythm
2) Angina pectoris (dec of O2 to the heart)
3) Overstimulation produces tachycardia, dysrhythmias


69. Therapeutic Applications:
 Limited to the lungs and uterus
 1) Asthma – bronchodilation
 2) Delay of preterm labor/relax uterine smooth
muscle.
Adverse Effects:
1) Hyperglycemia – Main concern is pt. with
diabetes
2) Tremor – b/c of activation of skeletal muscle

70. Therapeutic Applications:
 Dopamine is ONLY NT that can activate
dopamine receptors.
 Cause dilation of the vasculature of the kidneys
which dec. risk of renal failure.
 Enhances cardiac performance b/c it acts on
beta1 in the heart.

71. Have a high specificity for their receptors
2 Groups

1)
Alpha adrenergic blockers:
HTN - Most useful for alpha1 blockade of blood vessels

Alpha1 blockade is also good for benign prostatic hyperplasia

Pheochromocytoma – catecholamine secreting tumor in the
adrenal medulla

Reynaud's dz – vasospasm in toes and fingers so prevent
vasoconstriction
Adverse Effects:

Orthostatic hypotension

Reflex tachycardia

Nasal congestion

Inhibit ejaculation


72. 2) Beta Adrenergic blockers:

Biggest therapeutic effects from beta1 blockade in the heart
1) Reduced heart rate
2) Reduced force of contraction
3) Reduced velocity of impulse conduction
Therapeutic Application:

Angina pectoris
Heart failure

HTN
Hyperthyroidism

Headaches
Stage fright

Cardiac dysrhythimias Glaucoma
Adverse Effects:

Rebound cardiac excitation
AV heart block

Reduced cardiac output
Bradycardia

Heart failure

73. Drug
Receptor
Receptor
Phentolamine
Alpha1
Alpha2
Phenoxybenzamine
Alpha1
Alpha2
Alfuzosin
Alpha1
Doxazosin
Alpha1
Prazosin
Alpha1
Terazosin
Alpha1
Tamsulosin
Alpha1

74. Drug
Receptor
Receptor
Carteolol
Beta1
Beta2
Carvedilol
Beta1
Beta2
Labetalol
Beta1
Beta2
Nadolol
Beta1
Beta2
Penbutolol
Beta1
Beta2
Pindolol
Beta1
Beta2
Propranolol
Beta1
Beta2
Timolol
Beta1
Beta2
Sotalol
Beta1
Beta2
Atenolol
Beta1
Betaxolol
Beta1
Bisoprolol
Beta1
Esmolol
Beta1
Metoprolol
Beta1
Acebutlol
Beta1