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Pharm #2 > L14-16 adrenergic agonists and antagonists > Flashcards

L14-16 adrenergic agonists and antagonists Flashcards

1
Q

pre-ganglionic fibers release

A

Ach

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2
Q

post-ganglionic fibers release

A

parasympathetic : Ach

sympathetic : Norepinephrine (adrenergic)

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3
Q

adrenal medula releases

A

Mostly Epi and some NE into the circulation

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4
Q

post-ganglionic sympathetic fivers that innervate the sweat glands release

A

Ach (exception)

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5
Q 
Main functions of the parasympathetic NS on:
eye
heart
bronchioles
GI tract
Bladder
A

eye - constrict the circular (sphincter) muscles of the pupil (miosis)

heart - innervates the sinoatrial node to reduce HR, and the AV node to slow conduction

bronchioles - constricts smooth muscle of the bronchi

GI tract - promotes secretions and motility

Bladder - causes constriction of the detrusor muscle and emptying

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6
Q

Main functions of the sympathetic NS on:
eye
heart
bronchioles

A

eye - innervates the radial(dilator) muscle causes mydriasis and the ciliary body to stimulate production of aqueous humor

heart - accelerated sinoatrial node pacemaker depolarization (increases HR)

bronchioles - relaxation of the smooth muscle lining

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7
Q

How does sympathetic innervation affect HR

A

increases the inward calcium current to promote faster spontaneous depolarization (phase 4)

lowers the threshold for activation

stimulates a greater calcium influx into myocytes increasing the contractile force of depolarization.

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8
Q 
Main functions of the sympathetic NS on:
Blood vessels
GI tract
Bladder
metabolic fuctions
A

Blood vessels - contraction and relaxation depending on the receptor

GI tract - decreased motility

Bladder - inhibits emptying by contracting sphincters

metabolic functions - increase blood sugar

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9
Q

factors determining the response to NT receptor binding

A
  1. type of receptor
  2. secondary messenger system
  3. cell machinery (cell type)
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10
Q

effects of inhibition of re-uptake

A

potent sympathomimetic effects - signifies the importance of re-uptake in termination of the normal NTs affects

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11
Q

Sympathomimetic drugs

A

stimulate the sympathetic system

interact with adrenergic receptors directly

endogenous ligands for adrenergic receptors are epinephrine, norepinephrine, and dopamine

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12
Q

alpha1 receptors where they are found and what they do

A

contracts vascular smooth muscle

contracts pupillary dilator muscle (mydriasis)

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13
Q

Beta1 receptors where they are found and what they do

A

heart - stimulates rate and force

juxtaglomerular cells - stimulates renin release

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14
Q

Beta2 receptors where they are found and what they do

A

respiratory, uterine, and vascular smooth muscle - relaxes

somatic motor nerve terminals (voluntary muscle) - causes tremor

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15
Q

Dopamine1 receptors where they are found and what they do

A

renal and other splanchnic blood vessels - relaxes/ reduces resistance.

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16
Q

process of vascular smooth muscle contraction

A
  1. NE or EPI (or another a1-agonist) binds the a1-adrenergic receptor on vascular smooth muscle
  2. Gaq subunit activates PLC which liberates IP3 and DAG
  3. IP3 activates IP3 receptor opening a Ca release channel from the SR and allowing the release of Ca- stimulation smooth muscle contraction
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17
Q

alpha2 receptors in nerve terminals

A

pre-synaptic alpha2 receptor activation decreases NT release.

  1. binding of alpha2 inhibits adenylyl cyclase > reduces cAMP
  2. reduced activation of PKA
  3. reduced calcium influx during membrane depolarization
  4. reduced vesicular release of NT
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18
Q

how does B1 receptors have a positive chronotrophic effect

A

activation of adenylyl cyclase and increase of cAMP can activate PKA– promoting phosphorylation of Ca channels leading to increased inward Ca current and faster nodal depolarization to the firing threshold

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19
Q

how does B1 receptors have positive inotrophic effects

A

increased cAMP > increased PKA > phosphorylation of L-type Ca channels > more Ca influx > larger trigger signal for release of Ca from the SR

more Ca also gets stored in the SR increasing the Ca release for the next trigger.

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20
Q

how does B2 receptors cause vascular smooth muscle relaxation?

A

cAMP activates PKA which phosphorylates and INACTIVATES myosin light chain kinase (MLCK).

Phosphorylated MLCK has a lower affinity for Ca-calmodulin decreasing its ability to phosphorylate myosin and allow cross-bridge formation.

overall: reduced smooth muscle contraction

highly expressed on bronchi and some vascular beds and therefore regulates the degree of airway constriction and peripheral vascular resistance

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21
Q

role of peripheral a2-adrenergic receptors

A

produce peripheral vasoconstriction (opposite mechanism of B2 receptors- inhibits adenylyl cyclase and cAMP)

inhibition of PKA leads to activation of MLCK and vascular smooth muscle constriction

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22
Q

isoproterenol (ISO)

A

synthetic catecholamine with large substitution that gives it increased affinity for beta receptors

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23
Q

efficacy at the a1-adrenergic receptors

A

epi > (or =) NE&raquo_space;isoproterenol

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24
Q

efficacy at the a2-adrenergic receptors

A

epi > (or =) NE&raquo_space;isoproterenol

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25
efficacy at the B2-adrenergic receptors
isoproterenol > EPI >> NE
26
efficacy at the B1-adrenergic receptors
Isoproterenol > EPI = NR
27
systolic pressure is mostly affected by
CO (adrenergic receptors in the heart)
28
diastolic pressure is mostly affected by
TPR (arterial vasoconstriction, adrenergic receptors on the vasculature)
29
epinephrine at low doses
B-receptor effects predominate B2 receptor activations causes peripheral vasodilation--decreasing diastolic BP B1 receptor activation has positive inotrophic (force) and chronotropic (HR) effects --- increasing CO and systolic BP
30
epinephrine at high doses
a1 receptor activation predominates (more receptors) -- peripheral vasoconstriction = elevated systolic and diastolic pressures
31
epinephrines effect on mean blood pressure
low dose- slight increase (bigger pulse pressure) | high dose- large increase
32
epinephrines affect on bronchiles
B2 receptors - bronchodilation | a1 receptor - decrease in bronchiole secretions
33
epinephrines toxicities
arrhythmias (a1 due to potential for very high BP)
34
epinephrine stimulates which receptors
a1, a2, B1, B2
35
Norepinephrine stimulates
a1, a2, B1
36
NE effects
Cardiovascular - due mostly to a1 activation: vasoconstriction (increased TPR and diastolic BP). B1 positive inotropic and chronotropic effects (increase systolic BP) large rise in BP leads to baroreceptor response and DECREASE in HR (dominates over the direct chronotropic effects) Overall: MAP increases (NE has a limited affinity for B2 receptors so there is little change in bronchiole smooth muscle)
37
NE toxicities
ischemia (preexisting could become gangrene)
38
contraindication for NE
pre-existing excessive vasoconstriction and ischemia
39
dopamine receptor affinities
stimulates D1 at low concentrations but can also stimulate B1 and a1 and a2 receptors at higher concentrations
40
domamine effects
low infusion rates : D1 receptor - decreased TPR medium : actives B1 receptors leading to increased cardiac contractility and HR high: stimulates alpha receptors leading to increased BP and TPR
41
dopamine toxicity
low infusion rate: hypotension high infusion rates: ischemia
42
dopamine contraindication
uncorrected tachyarrhythmias
43
advantage of dopamine vs Epi
dopamine vasodilates blood vessels to certain organs such as the kidneys which can protect them from ischemia in shock while constricting other vessels to raise BP
44
example of non-selective B-adrenergic agonist
isoproterenol
45
effects of non-selective B-adrenergic agonist
CV: B1- positive inotrophic and chronotrophic. B2 peripheral vasodilation. Overall- slight decrease in MAP (may have small increase in systolic initially followed by decrease) Bronchioles: dilation (B2)
46
toxicity effects of B-adrenergic agonis (Isoproterenol)
tachyarrhythmias
47
contraindications of non-selective B-adrenergic agonist (isoproterenol)
arrhythmias
48
example of a selective B1 agonist
Dobutamine (receptor affinity is B1>B2>a)
49
Selective B1 receptor agonist effects
CV: increased CO-- unique in that positive inotropic effect (contractility) > positive chronotropic (HR) effect (due to lack of B2 mediate vasodilation and reflex tachycardia) high doses- B2 activation could lead to hypotension with reflex tachycardia
50
dobutamine toxicity (B1 selective agonist)
hypotension (especially at doses activating B2)
51
effects of selective B2 adrenergic agonists
CV: negligible usually but can cause some B1 agonist-like response Bronchioles- bronchiodilation
52
toxicity
B1 activation- tachycardia, tolerance (long term use) B2-skeletal muscle tremor (activation of B2 receptors on pre-synaptic nerve terminals of cholinergic somatomotor neurons)
53
therapeutic uses of selective B2 agonist
bronchospasms (acute asthma) and obstructive airway disease
54
examples of selective B2 adrenergic agonists
terbutaline and albuterol
55
example of selective a1 adrenergic agonist
phenylephrine
56
effects of selective a1 adrenergic agonists
CV: peripheral vasoconstriction and increased BP, activates baroreceptor reflex decreasing HR Ophthalmic: dilates pupil Bronchioles: decrease bronchial (and upper airway) secretions
57
contraindication of selective a1 agonists
pre-existing excessive vasoconstriction ans ischemia
58
benefits of phenylephrine
longer half life (not a catecholamine therefore not degraded by COMT) allowing it to be applied directly to where it is needed-- topically or inhaled IV during surgery to increase BP
59
toxicity of a1 adrenergic agonists
hypertension
60
Selective a2 adrenergic agonists example
clonidine
61
clonidine effects
CV: peripheral vasoconstriction and slight increase in BP, crosses the BBB to cause reduced sympathetic outflow which reduces vasoconstriction and BP. OVERALL: reduction in BP reduces tonic excitatory input to the sympathetic cells reduces sympathetic output to vascular smooth muscle
62
toxicity of clonidine
Dry mouth, withdrawal after chronic use can lead to life-threatening hypertensive crisis
63
function of indirectly acting sympathomimetics
increase the concentration of endogenous catecholamines in the synapse and circulation via either: 1. release of cytoplasmic catecholamines 2. blockade of re-uptake transporters
64
examples of releasing agents
amphetamine, methamphetamines, methylphenidate, ephedrine, pseudoephedrine, tyramine
65
amphetamine like drugs method of action
are taken up by re-uptake proteins reverse the re-uptake mechanism causes release of NT in a calcium-independent manor easily cross the BBB- high abuse potential due to reinforcing effects of central dopamine release
66
effects of releasing agents
CV: due to NE release, a receptor- peripheral vasoconstriction. B-receptor positive inotropy and contractility CNS: stimulant, anorexia agent
67
toxicity of releasing agents
tachycardia
68
therapeutic uses of releasing agents
ADD, narcolepsy, nasal congestion
69
contraindications of releasing agents
rx with NAO inhibitors within the previous 2 weeks (will increase the effects)
70
3 categories of beta blockers
``` non selective (B1 and B2) cardiac selective (B1) partial agonist (B1 and B2) ```
71
examples of non-selective B-Blockers
propranolol, nadolol, timolol
72
disadvantage of non-selective B-Blockers
potentially harmful side effects for patients with respiratory disease
73
Effects of non-selective B-Blockers
CV: reduced HR and contractility, reduced renin release leads to reduced vasoconstriction Bronchioles: bronchiole constriction in those with asthma or chronic obstructive pulmonary disease
74
uses of non-selective B-blockers
hypertension, angina, glaucoma, heart failure, arrhythmia
75
toxicity associate with non-selective B-blockers
bronchospasm asks symptoms of hypoglycemia, CNS effects including insomnia and depression, some can raise triglycerides, bradycardia
76
contraindications with non-selective B-blockers
Bronchial Asthma*** | sinus bradycardia, heart block, cariogenic shock
77
examples of cardioselective B1-blockers
metoprolol, atenolol, esmolol
78
effects of cardioselective B1-blocker
CV: same as nonselective: reduced HR and contractility, reduced renin release leads to reduced vasoconstriction
79
toxicity of cardioselective B-blockers
typically mild and transient- depression, insomnia, hypotension*, bradycardia
80
contraindications for cardioselective B-Blockers
heart block, cardiogenic shock
81
partial agonists B-blockers example
pindolol
82
pindolol acts on which receptors
B1 and B2
83
benefits to pindolol
good when hypertension is due to high sympathetic output- they have less bradycardic effect bc some B signal still remains used when patients are less tolerant of bradycardia effects
84
effects of partial agonist B-blocker
CV: reduced HR and contractility, reduced renin release leads to reduced vasoconstriction (same as others)
85
therapeutic uses
hypertension in those who are less tolerant of bradycardia and reduced exercise capacity cause by other beta blockers
86
toxicity of partial agonist B-blockers
bronchospasm asks symptoms of hypoglycemia, CNS effects including insomnia and depression, some can raise triglycerides, bradycardia(less severe)
87
non selective alpha-adrenergic antagonists example
phenoxybenazamine (irreversable) | phentolamine (reversible)
88
characteristics of a reversible antagonist
Emax remains the same but ED50 increases
89
effects of nonselective a-receptor antagonists
CV: inhibit vasoconstriction (decreases BP), increased inotropy and chronotropy due to blockade of pre-synaptic a2 receptor. reflex increase in NE release- unmasks vasodilatory effect of EPI
90
toxicity of nonselective alpha antagonists
prolonged hypotension, reflex tachycardia, nasal congestion
91
examples of selective a1-receptor blockers
prazosin, doxazosin, terazosin
92
effects of selective a1-receptor blockers
``` inhibit vasoconstriction (decreased BP) less cardiac stimulation than non-selective a-blockers due to preservation of a2 adrenergic function ```
93
therapeutic uses of selective a1-antagonists
hypertension, benign prostatic hyperplasia (relaxes the muscle to help with urination)

Pharm #2 (13 decks)

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