Year 1 Physiology > Autonomic > Flashcards

Autonomic Flashcards

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1
Q

What is the final common pathway linking the CNS to skeletal muscles?

A

Alpha motor neurons

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2
Q

What serves as the final common pathway from the CNS to visceral targets?

A

Sympathetic and parasympathetic neurons

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3
Q

Where is the myenteric (Auerbach’s) plexus?

A

Between external longitudinal and deeper circular smooth muscle layers of GI tract

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4
Q

What is the function of the myenteric (Auerbach’s) plexus?

A

GI motility

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5
Q

Where is the submucosal (Meissner’s) plexus?

A

Between circular muscularis mucosae

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6
Q

What is the function of the submucosal (Meissner’s) plexus?

A

Controls ion and fluid transport

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7
Q

Can the enteric nervous system function without input from the ANS?

A

Yes

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8
Q

What organs/tissues receive only sympathetic innervation?

A
  1. Hair follicles2. Sweat glands3. Liver4. Adrenal glands5. Kidneys6. Blood vessels (mostly)
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9
Q

All somatic nerves release what NT?

A

Ach

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10
Q

All preganglionic fibers in the ANS release what NT?

A

Ach

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11
Q

Sympathetic postganglionic fibers release what NTs?

A
  1. Adrenergic (Epi/NE) 2. Dopaminergic (renal vascular smooth muscle) 3. Exception - thermoregulatory sweat glands (muscarinic, Ach)
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12
Q

What are the steps of cholinergic transmission?

A

1 .Synthesis of NT at presynaptic terminals2. Storage of NT 3. Release of NT 4. Action at receptor sites5. Termination of transmitter action

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13
Q

What are the steps of Ach synthesis?

A
  1. Choline transport into neuron from extracellular fluid via sodium dependent choline transporter CHT 2. Acetyl CoA synthesized in mitochondria 3. Ach synthesized from choline and acetyl CoA via choline acetyltransferase (ChAT)
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14
Q

What drugs inhibit the choline transporter?

A

Hemicholiniums

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15
Q

What enzyme transports choline from the extracellular fluid into the neuron?

A

Choline transporter CHT (sodium dependent)

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16
Q

What enzyme synthesizes Ach?

A

Choline acetyltransferase (ChAT)

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17
Q

What are the steps of Ach storage?

A
  1. Ach transported into storage vesicle by vesicle associated transporter VAT 2. Vesicles held on inner surface of terminal via vesicle associated membrane proteins (VAMPs) and synaptosome associated proteins (SNAPs)
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18
Q

What drug inhibits VAT?

A

Vesamicol

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19
Q

What else is stored in the Ach storage vesicle?

A
  1. Peptides2. ATP 3. Proteoglycan
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20
Q

What are the steps of Ach release?

A
  1. Depolarization of nerve terminal2. Voltage dependent calcium entry3. Calcium binds calmodulin and activates VAMPs and SNAPs4. Vesicle fusion and NT release
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21
Q

What step in Ach release does Botox inhibit?

A

VAMP activity (removal of two amino acids)

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22
Q

What are the steps of NT termination of action?

A
  1. Rapid hydrolysis of Ach via acetylcholinesterase2. Choline reuptake into terminals
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23
Q

What are the three fates of Ach following release?

A
  1. Bind to receptors2. Degradation into choline and acetate3. Binds to presynaptic terminal
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24
Q

What drug inhibits AchE?

A

Neostigmine

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25
What are the two categories of cholinergic receptors?
1. Muscarinic2. Nicotinic
26
What are the properties of muscarinic receptors?
1. G protein coupled 2. 5 subtypes (M1-M5)3. Signaling depends on type of G protein receptor associated with it
27
What are the M receptor - G protein couplings?
1. M1 - Gq2. M2 - Gi/o3. M3 - Gq
28
What is the result of activation of Gq associated M receptors?
Increase in calcium concentration and activation of PKC
29
What is the result of activation of Gi/o associated M receptors?
Decrease in intracellular cAMP concentration and decreased PKA activity
30
What are the properties of nicotinic receptors?
1. 5 subunit transmembrane ion channel 2. Channel is closed when no Ach is bound3. When Ach is bound to 2 alpha subunits a conformational change results in Na and K flowing down respective electrochemical gradients 4. Sodium influx produces an excitatory postsynaptic AP
31
What muscles in the eye use M3 receptors?
1. Sphincter pupillae2. Ciliary muscle (also has B2)
32
The sphincter pupillae and ciliaries muscles have what type of receptor?
M3
33
The SA and AV nodes have what type of receptor?
M2
34
The bronchioles and lung glands have what type of receptor?
M3
35
The stomach and intestine have what type of receptors?
M3
36
The GI glands have what type of receptor?
M1
37
The bladder has what type of receptor?
M3
38
Sphincters have what type of receptor?
M3
39
Endothelial cells have what type of receptors?
M3
40
What is the effect of M3 activation in the eye?
1. Constricted pupil / miosis 2. Accommodation for near vision
41
The radial (dilator) muscle of the eye is controlled by what type of nerve fibers?
Sympathetic a1 fibers
42
The ciliary epithelium has what type of receptors?
1. B1 and B2 2. Activation increases aqueous humor production
43
How does muscarinic receptor activation work in the heart?
1. Ach interacts with M2 receptors linked via Gi/o to a K channel2. K channel opening leads to hyperpolarization 3. Voltage dependent opening of pacemaker Na current channels (If) is shifted to more negative potentials 4. Phosphorylation of L type calcium channels is reduced 5. cAMP and PKA is reduced - inhibition
44
What are the tissue effects of M2 activation in the heart?
1. SA node - decreased heart rate, negative chronotropy2. AV node - decreased conduction velocity3. Atrial muscle - decreased atrial contraction4. Ventricular muscle - decreased ventricular contraction
45
What are the tissue effects of M3 activation in the lungs?
1. Bronchi and bronchioles - contraction, bronchospasm2. Brochiolar submucosal glands - secretion, narrow lumen
46
What are the tissue effects of muscarinic receptor activation in the GI tract?
1. Stomach (M3) - motility, cramps2. Glands (M1) - secretion3. Intestine (M3) - contraction, diarrhea, involuntary defecation
47
What are the effects of M3 activation in the bladder?
1. Facilitates urination 2. Contracts detrusor muscle 3. Relaxes trigone 4. Inhibits contraction of sphincter
48
What controls visceral smooth muscle?
Only nerve input
49
What controls vascular smooth muscle?
1. Nerve input2. Endothelial factors
50
In intact endothelium, what does activation of M3 receptors do?
1. M3 activation increases calcium 2. Increased calcium stimulates eNOS to produce NO3. Vasodilation
51
What is the mechanism of M1 and M3 receptor activation?
1. Gq activates phospholipase C 2. Phospholipase C cleaves PIP2 into IP3 and DAG3. IP3 increases calcium levels4. DAG increases PKC levels
52
What is the mechanism for M2 receptor activation?
1. Gi activates adenylate cyclase2. Adenylate cyclase decreases cAMP3. Decreased cAMP leads to decrease PKA
53
How are catecholamines synthesized?
1. Via tyrosine - DOPA - dopamine - NE - Epi2. Via tyramine - NE
54
What does metyrosine do?
1. Blocks tyrosine hydroxylase activity2. DOPA cannot be made from tyrosine
55
What is the rate limiting step in catecholamine synthesis?
Conversion of tyrosine to DOPA
56
What is the final product in most sympathetic postganglionic neurons?
NE
57
Where is NE further converted to Epi?
1. Adrenal medulla 2. Certain areas of the brain
58
How are catecholamines stored?
Synthesized catecholamines transported into vesicles by vesicular monoamine transporter (VMAT)
59
What does reserpine do?
Inhibits vesicular monoamine transporter (VMAT) in catecholamine storage process
60
What does bretylium do?
1. Inhibits VAMPs in catecholamine release (sympathetic nerve endings)2. Analagous to botox
61
What are the fates of catecholamine termination of action?
1. Act on postsynaptic terminal2. Diffuse into blood stream3. Activate autoreceptors4. Brought back into nerve terminal by NET
62
What metabolizes catecholamines that diffuse into the blood stream?
Catechol-O-methyl transferase (COMT) in liver
63
What is the function of norepinephrine transporter (NET)?
1. Carries NE and similar molecules back into cell cytoplasm from synaptic cleft2. Inhibited by cocaine and tricyclic antidepressants
64
What effect do cocaine and tricyclic antidepressants have on catecholamine metabolism?
1. Inhibit NET2. Increased NT activity in cleft
65
What characterizes extraneuronal uptake in adrenergic receptors?
1. Accomplished via ENTs (extraneuronal transporters) 2. Corticosteroids inhibit ENTs and NETs
66
What are the fates of NE if reuptaken into the terminal?
1. Restored in vesicles2. Metabolized by MAO
67
What happens to NE concentration in a patient using MAO inhibitors?
1. Enhance availability of tyramine2. Tyramine induced NE release from sympathetic neurons may cause hypertensive crisis
68
What is the main metabolite of NE?
Methylhydroxymandelic acid
69
What is the mechanism of adrenergic a1 receptor activation?
1. Activates Gq protein 2. Activates phospholipase C3. Phospholipase C activation leads to IP3 and DAG4. IP3 stimulates release of sequestered calcium 5. Increased calcium activates protein kinases 6. End result in vasculature is constriction
70
Blockage of what receptor in vasculature will result in dilation (and decreased blood pressure)?
a1
71
What is the mechanism of adrenergic B receptor activation?
1. Activates Gs protein2. Stimulation of adenylyl cyclase 3. Increased rate of synthesis of cAMP
72
What is the mechanism of adrenergic a2 receptor activation?
1. a2 adrenoceptor ligands inhibit adenylyl cyclase by dissociating Gs into subunits 2. cAMP levels go DOWN 3. PKA levels go DOWN
73
What occurs in the eye following a1 activation?
1. Contract dilator pupillae muscle2. Dilate pupil
74
What occurs in the eye following use of a B1/B2 blocker?
Decreased aqueous humor production
75
What are the effects of a1 receptor activation in the radial muscle of the eye?
Contraction - mydriasis
76
What are the effects of a1 receptor activation in the skin and viscera arterioles?
1. Contraction 2. Increased TPR3. Increased afterload
77
What are the effects of a1 receptor activation in veins?
1. Contraction2. Increased venous return3. Increased preload
78
What are the effects of a1 receptor activation in the liver?
1. Increased glycogenolysis2. Increased blood glucose
79
What are the effects of a1 receptor activation in the vas deferens?
Ejaculation
80
What are the effects of a1 receptor activation in the bladder trigone and internal sphincter?
1. Contraction2. Urinary retention
81
What are the effects of a2 receptor activation in the prejunctional nerve terminal?
Decreased transmitter release and NE synthesis
82
What are the effects of a2 receptor activation in platelets?
Aggregation
83
What are the effects of a2 receptor activation in the pancreas?
Decreased insulin production
84
What are the effects of B1 receptor activation in the heart?
1. SA node - increased HR2. AV node - increased conduction velocity 3. Atrial and ventricular muscle - increased contraction force, conduction velocity, cardiac output, O2 consumption4. His-Purkinje system - increased automaticity and conduction velocity
85
What are the effects of B1 receptor activation in the kidney?
Increased renin release
86
What are the effects of B2 receptor activation in blood vessels?
Vasodilation - decreased TPR, diastolic BP, afterload
87
What are the effects of B2 receptor activation in the uterus?
Relaxation
88
What are the effects of B2 receptor activation in the bronchioles?
Dilation
89
What are the effects of B2 receptor activation in skeletal muscle?
Increased glycogenolysis - contractility
90
What are the effects of B2 receptor activation in the liver?
Increased glycogenolysis
91
What are the effects of B2 receptor activation in the pancreas?
Increased insulin secretion
92
What are the effects of domaminergic receptor activation in renal, mesenteric, coronary, and vascular tissues?
Vasodilation
93
What are the properties of homotropic interactions?
1. Presynaptic receptors whose ligands are the same as the NTs released by that nerve terminal 2. Acts powerfully at noradrenergic nerve terminals
94
What are the properties of heterotropic interactions?
1. One NT affects the release of another via actions on heteroceptors 2. Examples: NE affects Ach release and vice versa, myenteric plexus - NE/Epi vs Ach, heart - NE vs Ach
95
What is the denervation / hypersensitivity phenomenon?
1. If a nerve is cut and its terminals are allowed to degenerate, the structure supplied by it becomes supersensitive to the transmitter released by its terminals 2. Sustained blockade of ganglionic transmission / postsynaptic receptors render downstream target organs supersensitive to the ligand when the blocker is acutely removed
96
What is the mechanism of denervation / hypersensitivity?
1. Proliferation of receptors2. Loss of mechanisms for transmitter removal (no uptake) 3. Increased postjunctional responsiveness
97
What is cotransmission?
Neurons release more than one NT or modulator, each of which interacts with specific receptors and produces effects, often both pre- and postsynaptically
98
What are the functional implications of cotransmission?
1. One component of the cocktail may be removed or inactivated more slowly than the other - targets reached further from site of release with longer effects2. Differential release of one or other mediator may result from varying impulse patterns3. Differential effects of presynaptic modulators also possible
99
What are the main functions of the ANS?
1. Assist body in maintaining constant internal environment2. Accommodate coordinated responses to external stimuli
100
What are the feedback loops involved in autonomic reflexes of the heart?
1. ANS loop2. Hormonal loop
101
What is the mean arterial pressure?
1. Meeting point of the ANS loop and hormonal loop2. Primary controlled variable in cardiovascular function
102
What variables of cardiovascular function are controlled by the sympathetic nervous system?
1. Peripheral vascular resistance2. Heart rate3. Force4. Venous tone
103
What variable of cardiovascular function is controlled by the parasympathetic nervous system?
Heart rate
104
What is the effect of angiotensin II on cardiovascular function?
1. Directly increases peripheral vascular resistance2. Facilitates sympathetic effects
105
What is the result of increased total peripheral resistance (increased a1 activation) in the context of arterial BP?
Reflex bradycardia
106
What is the result of decreased total peripheral resistance (decreased a1 activation) in the context of arterial BP?
Reflex tachycardia
Year 1 Physiology
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