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ANS physiology Flashcards

1
Q

Which part of the ANS leads to every part of the body?

A

Sympathetic (unlike parasympathetic)

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2
Q

Location of all sympathetic neurons

A

lateral horn of gray matter from T1-L2

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3
Q

alpha1-AR

G protein:
Agonist:
Function:

A

G protein: Gq
Agonist: NE > Epi
Function: smooth muscle contraction

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4
Q

Beta1-AR

G protein:
Agonist:
Function:

A

G protein: Gs
Agonist: NE = Epi
Function: heart muscle contraction

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5
Q

Beta2-AR

G protein:
Agonist:
Function:

A

G protein: Gs and Gi
Agonist: Epi > NE (only epi)
Function: Smooth muscle vasodilation

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6
Q

M2-R

G protein:
Agonist:
Function:

A

G protein: Gi and K+
Agonist: ACh
Function: slow heart rate

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7
Q

M3-R

G protein:
Agonist:
Function:

A

G protein: Gq
Agonist: ACh
Function: BV vasodilation via NO

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8
Q

NE released works on ___ receptor on heart cell, causing an increase in these two factors and stimulates (contraction/dilation)

A

beta 1; inotropy and chronotropy; contraction

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9
Q

If you stimulate sympathetic, why does inotropy increase?

A

due to calcium

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10
Q

What are major effects if you increase inotropy?

A

decrease end systolic volume, (move to new starling’s curve) and increase stroke volume

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11
Q

What are the four major targets of PKA phosphorylation (from Gs cascade)? Effects?

A
  1. L-type Ca channel -increases open probability, more Ca coming in
  2. RYR receptors -increases its open probability , more Ca release from SR
    - —for every contraction, need equal and opposite relaxation—-
  3. PLB -allow for increase activity of SERCA pump, more can be pumped into SR and faster
  4. Troponin I -enhances relaxation effects of actin myosin filaments
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12
Q

If there’s an increase in calcium, there will be an increase in force of contraction. What agonist will give you a stronger contraction?

A

Beta1 adrenergic agonist

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13
Q

What happens if you give a beta1 adrenergic stimulation with NE?

A

Stimulate Aps

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14
Q

What is biggest effect of NE beta adrenergic on SA node action potentials? Step by step explanation

A

Recall that SA node action potential uses a If funny channel:

NE binds to Gs protein, increases cAMP, binds directly to HCN channel (If), increases open probability, more Na coming into cell, increase the slope, reaches threshold faster, more frequent APs

INCREASE IN SLOPE = BIGGEST EFFECT

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15
Q

What are the major effects of NE beta adrenergic on ventricular action potentials?

A
  • increase in calcium current I(Ca) –> increase in plateau stage due to more Ca coming in
  • increase K current –> slope of repolarization is steeper, so have a shortened APD
  • PKA can also phosphorylate K channels, which increases their activity

-results in faster and more frequent ventricular AP

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16
Q

What is Long QT syndrome?

  • mutation
  • effects on AP
  • what it causes
A
  • body cannot respond to increase stress
  • mutation in slow rectifying K channels, can’t respond
  • get high increase of plateau phase (Ca channels still work)
  • depolarization duration increases
  • when trying to stimulate next depolarization, still having leftover repolarization
  • mix up = arrhythmia
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17
Q

definition of inotropy

A

change in strength of muscular contraction (positive inotropy increases the strength of muscular contraction)

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18
Q

definition of chronotropy

A

change in heart rate

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19
Q

NE release on heart cells works on what two receptors? What are the effects? (3)

A
  • works predominantly on B1
    1. increases inotropy
    2. increases chronotropy
  • works on alpha1
    3. stimulates vasoconstriction
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20
Q

What causes an increase in vasoconstriction when NE is released?

A

alpha 1 adrenergic receptors stimulates Gq cascade –>MLCK –> phosphorylates myosin light chain –> smooth muscle contraction

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21
Q

When inotropy increases, what happens to stroke volume? Why?

A

SV increases:
As inotropy increases, end-systolic volume decreases (stronger contraction)

SV = end diastolic - end systolic (decreased) = bigger SV value

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22
Q

When inotropy increases, what happens to HR? CO?

A

increased inotropy causes an increase in stroke volume. Increased SV causes increase in HR and thus CO (recall CO = SV x HR)

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23
Q

How does NE/Epi release affect arterial pulse pressure?

A

-increases arterial pulse pressure

increases systolic pressure, slightly decreases diastolic pressure

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24
Q

How does Epi release affect MAP and SVR?

A

MAP = CO x SVR

MAP does not change! Even though CO increases, SVR decreases due to vasodilation (epi binds to beta2, causes smooth muscle vasodilation)

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25
How does NE release affect MAP and SVR?
see increase in MAP- Epi activates alpha1, which causes smooth muscle contraction, so SVR will increase in addition to CO.
26
sympathetic has (short/long) presynaptic and (short/long) post synaptic
short pre, long post
27
Sympathetic acts predominantly on what two receptors?
Beta 1 and alpha 1 receptors
28
How does sympathetic increase inotropy?
by increasing calcium
29
How does sympathetic increase chronotrophy?
By affecting SA node
30
Does sympathetic affect ventricular AP?
Yes--affects I(Ca) and I(K), results in faster and more frequent APs
31
Sympathetic increases (vasoconstriction/vasodilation)
vasoconstriction
32
Sympathetics increase ___ due to increase in SV and HR
CO
33
Sympathetics increase ___ due to increased SVR
MAP
34
Main effects on ACh (3)
1. reduces inotropy 2. reduces heart rate 3. stimulates vasodilation
35
How does ACh reduce inotropy + heart rate
Ach binds to Gi, decrease cAMP activity, all phosphorylation decreases, slows down heart rate
36
What is effect of ACh on SA node action potential? How?
Decreases chronotropy. - ACh affects the I(K) potassium channels- activation of I(K) causes hyper-repolarization and lower repolarization - ->takes longer to reach threshold, shortens APD - ->get thinner and fewer APs
37
How does ACh stimulate vasodilation?
Binds M3-R, receptor produces eNOS in endothelial to synthesize NO. NO is a relaxan/vasodilator via stimulation of protein kinase G (PKG) endothelial NO synthetase (eNOS) is an isoform of NO
38
In measuring heart rate, (parasympathetic/sympathetic) tone predominates
parasympathetic
39
In measuring heart rate, (Vagal/Sympathetic) affects are faster. Why?
Vagal -parasympathetics acts through Gi which acts on K channel--see immediate change meanwhile in sympatehtic, need to generate cAMP, activate kinase, phosphorylate--all of which take time to reach maximal stimulation
40
Parasympathetic have (short/long) presynaptic and (short/long) post synaptic
long pre, short post
41
Parasympathetic act predominantly on which receptor?
Muscarinic 2-R to slow down heart rate
42
Parasympathetics (increase/decrease) inotropy by what to mechanisms?
Decerase 1. decrease phosphorylation 2. activating K+ channels
43
What initiates the baroreceptor reflex? How does it affect heart rate?
Sudden changes in arterial (phasic) blood pressure, cause inverse change in HR
44
Where are the afferent receptors located for baroreceptor feedback?
NTS-nucleus tract solitarius in the medulla
45
As sinus pressure increases, (sympathetic/parasympatheitc) stimulation increases
Parasympathetic increases while sympathetic stimulation decreaese
46
Baroreceptor response happens constantly in our phasic blood pressure. Explain how
Phasic blood pressure during systole (increase in pressure) and diastole (decrease in pressure) - during high systole, increase vagal stimulation - during diastole, vagal stimulation decreases
47
How can baroreceptors affect heart rate?
as increase pressure >> decrease HR | (decrease sympathetics and increase vagal stimulation). baroreceptor tries to maintain normal
48
Central chemoreceptor (location and function)
medulla, detect changes in pH of cerebrospinal fluid to hypercapnic hypoxia (too much CO2 in blood)
49
Peripheral chemoreceptor (location and function)
Aortic body: detect changes in blood O2 and Co2 | Carotid body: detects O2, CO2, and pH
50
Peripheral chemoreceptors i.e. arterial pO2, arterial pCO2, and hydrogen ion (+/-) medullary vagal center, which (+/-) heart rate
(+) medullary vagal center, (-) heart rate
51
stimulated medullary vagal center (+/-) breathing rate, which will (+/-) heart rate
(+) breathing rate, (+) heart rate can see that peripheral chemoreceptors activate medullary vagal center, which directly decreases heart rate and indirectly incerases heart rate. A bit counteractive but net effect: only small heart rate drop
52
Bainbridge reflex
an increase in heart rate due to an increase in central venous pressure
53
In the Bainbridge reflex, how is increased blood volume detected? Location?
By stretch receptors in both atria and ventroatrial junctions
54
What are effects of sympathetic stimulation on the kidney?
Renin gives rise to AngII, causes following: - stimulates cardiac and vascular hypertrophy - increased blood volume, increased CO, increased arterial pressure
55
What happens when you stand up? Go through following: - venous return, central venous perssure, ventricular preload - stroke volume - CO and MAP - baroreceptor firing - sympathetic and vagal stimulation - vasoconstriction, inotropy, and chronotropy - CO and SVR and MAP
- pooling of blood in legs due to gravity - decrease venous return etc. - decrease stroke volume - decrease CO and MAP (SVR unaffected) - decreased baroreceptor firing - decrease vagal stimulation (since lower pressure) - increase sympathetic stimulation in medulla - increase vasoconstriction, inotropy, and chronotropy - increase CO and SVR - increase MAP
56
baroreceptor reflex: | -as sinus pressure increases, vagal/sympathetic increases, while vagal/sympathetic decreases
vagal activity increases sympathetic activity decreases if pressure increases, want to calm it down by activating rest and digest!
57
When you begin to exercise, causes an increase sympathetic stimulation so that you can increase blood flow to skeletal muscle?
baroreceptors decrease their firing rate (lower pressure will decrease vagal stimulation and increase sympathetic stimulation --> increase vasoconstriction, inotropy, chronotropy, CO, SVR, MAP, bingo!)
58
epinephrine (non-selective agonist) activates what receptor(s)?
alpha and beta receptors
59
What effect does Epi have on BP? Any predominance? How is this different than norepinephrine?
BP increases, dominant effect on systolic pressure. NE causes an increase in systolic AND diastolic blood pressure
60
What effect does Epi have on bronchii? Reasoning?
Dilates bronchii (fight or flight, increase volume of air space since want to run!)
61
Two main uses for epinephrine:
1) treatment of anaphylactic shock = severe allergic reaction 2) local anesthetics (increases duration, reduces bleeding
62
Norepinephrine (noradrenaline) activates what receptor(s)?
activates mostly alpha receptors
63
NE is a very potent vasopressor (epi is one also, but clinical uses are limited). What is this function used to treat?
NE used as a severe shock treatment
64
Two uses of alpha1 selective agonists and how they work
alpha 1 receptors, Gq protein - treatment of hypotensive state--vasoconstriction increases blood pressure (methoxamine) - local vasoconstrictor nasal decongestant--increase smooth muscle contraction around arterioles, allows more space for airway passage so you can breathe better, especially if sinuses are swollen (phenylephrine)
65
How do alpha2 selective agonists work to treat hypertension? (their function is smooth muscle contraction/inhibit of NT release)
they inhibit presynaptic alpha2 receptors in the cardiovascular control center in the CNS ---> reduce sympathetic activity --> decrease BP
66
Beta1 receptors are mostly found in the ____
heart
67
two main functions of beta1 receptors:
1. increase contractility = positive inotropy | 2. increase heart rate = positive chronotropy
68
beta2 receptors are located in _____
respiratory system in bronchial smooth muscle
69
Main function of beta2 receptor agonists
produce bronchial dilation
70
Main effect of beta1 selective agonists
strong inotropic effect (contractility) but little chronotropic effect (HR) ---> increase in cardiac output without significant increase in heart rate (dobutamine)
71
Dobutamine, a Beta1 selective agonist, is a mimic of what?
Exercise--increase in cardiac output without significant increase in heart rate
72
beta2 selective agonists target predominantly the _____
respiratory system
73
What is a clinical application of Beta2 selective agonists?
Asthma (smooth muscle dilation, need to get air to lungs) -drugs end in -terol - terenol
74
What do alpha selective ANTAGONISTS (blockers) promote?
Alpha1 is responsible for contraction, so if blocking this, it will promote vasodilation
75
effect of alpha-selective antagonists
decrease in blood pressure (blocks vasocontraction --> get vasodilation --> decreased peripheral resistance --> decrease blood pressure
76
Clinical applications of alpha-selective antagonists
hypertension, urinary retention (since promotes decrease in blood pressure)
77
Effects of alpha2 selective ANTAGONIST
enters CNS --> increased sympathetic output --> increased HR, BP, can cause severe tremors found in many weight loss products--not good!
78
What would beta2 selective ANTAGONISTS do? Why do they mostly have an "undesired side effect?"
They would trigger bronchial constriction --> no clinical use What we want is to antagonize beta 1 receptors
79
Effect of Beta1 selective ANTAGONISTS? Clinical Applications?
beta1 receptors cause heart muscle contraction, so an antagonist would cause heart muscle relaxation - hypertension, cardiac dysrhythmias, MI, heart failure, tremor, "stage fright" - propranolol, -olols

Year 1 (48 decks)

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