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47 Cards in this Set

  • Front
  • Back
does the ANS regulate fast or slow, long term or short term
FAST
short term modulation
Explain the 3 influences the ANS has:
1. Chronotropicity
2. Dromotropicity
3. Inotropocity
1. Chronotropicity: HR (SA node)
2. Dromotropicity: Velocity of conduction (AV)
3. Inotropocity: strength of contraction
what is the name of the influence that alters the AV node
dromotropicity, conduction velocity
what is the name of the influence that alters the SA node
chronotropicity, HR, rate of rhythem
what is the name of the influence that alters the contractility
inotropicity, contractility, strength of contraction, rate of force of development
what heart structures does the SNS innervate
1. SA
2. AV
3. Atria/Vent myocardium
In general what do the left SNS fibers do? Right SNS?
Left SNS: contractility of myocardium

Right SNS: Rate, Conduction, adrenal medulla
what NT are released by SNS
Pregang
Postgang

Adrenal medulle?
Pre: ACh
Post: NE

Adrenal: epi
How is HR increased?
SNS/PNS
Receptor
Location
NT

Influence
SNS RIGHT Side
B1
SA node
NE

**chronotropicity
How is Conduction velocity increased?
SNS/PNS
Receptor
Location
NT

Influence
SNS, RIGHT side
B1
AV Node
NE

Dromotropicity
How is contractility increased?
SNS/PNS
Receptor
Location
NT

Influence
SNS, LEFT side
B1
Vent Myocardium
NE

Inotropic
what N carries PNS?
distinguish R and L branches
Vagus

R: SA node
L: AV node
where do post gang parasymp act?
nodal tissue
conductile tissue

**slight atrial myocardium innervation
The SA node receives innervation from where (SNS, PNS)
SNS: Right
PNS: Right
The AV node receives innervation from where (SNS, PNS)
SNS: Right
PNS: Left
what is the NT for PNS, pre/post

What is the NT for SNS, pre/post
PNS
Pre and Post: ACh

SNS:
Pre ACh
Post: NE
What is an ACh agonist
atropine, will inhibit Muscarinic (PNS) receptors
what effect will M2 receptors have on the heart. what division of ANS. What NT
PNS
ACh

Decrease HR (SA)
Decrease Conduction (AV)
Decreased Contractility
Where are B1 and B2 located? what division of ANS
SNS

B1: Heart, conductile & cantractile
B2: Coronary Vascular SM (dilate)
what does the a1 receptor do?
Constricts Vascular SM
NE
SNS
What receptors have antagonistic effects on Vacular SM
a1: constrict vascular SM

b2: dilate vascular SM
what is the major PNS receptor for cardiac stuff? where is it located, what effect does it have, what receptor has opposite effects
M2
heart (SA, AV, conctractile?)
Decreases, HR, Decreases AV conduction, Decreases contractility
ACh

B1 in the heart does the opposite
what is the most important SNS cardiac receptor subtype. what does it do?
B1

Increase HR
Increase Contractility
Increase conduction in AV node
NE
what NT inhibits release of NE
What NT inhibits release of ACh
ACh
NE

**ACh and NE have opposite effects, one will inhibit the other. This is done presynaptically
What G protein does SNS activate? PNS?
SNS: B1, Gs

PNS: M2, Gi
How is chronotropicity altered via ANS?

**chronotropicity, HR, SA node
SNS:
B1 to increase HR, Gs, increased Na funny conductance to increase the slope of pacemaker potential

PNS: M2, decreases slope of pacemaker but increasing K conductance, hyperpolarize membrane so its harder to reach threshold, K-Ach
how is the slope of the pacemaker potential increased
B1 SNS Increase HR
increases Na conductance (funny current) to increase the rate of depolarization
SA node
Chronotropicity
how is the slope of the pacemaker decreased
M2 PNS, Decrease HR
Increase conductance to K+, decrease Na funny conductance, when K+ increases the membrane becomes hyperpolarized and its hard to have AP

**HR decreases, PP increases
how does ANS alter dromotropicity?

**conduction through AV
SNS:
B1, enhanced conduction through AV, increased upstroke due to Ca, increased PKF conduction, decreased PR interval

PNS:
M2, decreased conduction through AV, increased K conductance, decreased Ca conductance, decreased upstroke, increased PR
How is conduction velocity decreased
Dromotropicity
AV node
PNS

**decreased Ca conductance, increased K conductance, decreased upstroke, increased PR
how is conduction velocity increased
dromotropicity
AV node
SNS

**increased rate of doastolic depolarization, decreased PR interval, increased Upstroke (increased Ca conductance), increased PKF conduction
How does ANS alter Inotropicity

**contraction
SNS:
b1, increase contractility, increase cAMP, Pi sarcolemma channels to allow more Ca in and Ca induced Ca release, increased release of Ca from SR, increased Ca clearance for faster relaxation (phospholamban)

PNS:
M2 decrease contractility in atria by decreasing Ca conductance
how is calcium clearance/reuptake increased? what does this do to contractility?
Increases contractility, faster relaxation

1. increased SR CaATPase, more reuptake, more Ca available for next release

2. increased SA Ca ATP, phospholamban is Pi to increase its activity
what are the effects of positive inotropicity (SNS) on P when V is constant
increased pressire
Ne increases the velocity of mm fiber shortening, what effect does this have on contraction
increases
how are SNS PNS related
both are tonically active, one will win out

**at rest PNS wins
what branch of ANS is more active at rest
PNS
b1
Where is it
what does it do
what does it release

What receptor acts in opposition
heart
increase HR
increase Contractility
Increase conduction velocity

NE

**M2 does opposite
a1
Where is it
what does it do
what does it release

WHat receptor acts in opposiotion
Vascular SM
Constriction
NE

**b2 acts against it
b2
Where is it
what does it do
what does it release

WHat receptor acts in opposiotion
Vascular SM
dilation
isoproterenol (NE)

**a1 does opposite
M2
Where is it
what does it do
what does it release

WHat receptor acts in opposiotion
heart
Decrease HR
Decrease contractility
Decrease conduction velocity
ACh

**B1 works in opposite ways
where is a1 located and what is its signal transduction path
a1: vascular SM, constriction

increase release of Ca from SR, increase Ca influx
where is a2 located and what is its signal transduction path
vascular SM

inhibit adenyly cyclase, decrease cAMP
what is the signal transduction path of b1
B1, in the heart, increase HR, conduction, contractility

increase adenyly cyclase and increase cAMP
what is the signal transduction path of b2
Vascular SM, constriction

activate adenyly cyclase and increase cAMP. also increase cAMP dependent kinase actibity
what is the signal transduction path of M2
M2 in heart, decrease HR, decrease conduction velocity, decrease contractility

**inhibit adenyly cyclase, decrease cAMP

**increase k conductance
what is the signal transduction path of M3
cause dilation

**increased intracellular Ca, increased NO production