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47 Cards in this Set
- Front
- Back
does the ANS regulate fast or slow, long term or short term
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FAST
short term modulation |
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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 |
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what is the name of the influence that alters the AV node
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dromotropicity, conduction velocity
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what is the name of the influence that alters the SA node
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chronotropicity, HR, rate of rhythem
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what is the name of the influence that alters the contractility
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inotropicity, contractility, strength of contraction, rate of force of development
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what heart structures does the SNS innervate
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1. SA
2. AV 3. Atria/Vent myocardium |
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In general what do the left SNS fibers do? Right SNS?
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Left SNS: contractility of myocardium
Right SNS: Rate, Conduction, adrenal medulla |
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what NT are released by SNS
Pregang Postgang Adrenal medulle? |
Pre: ACh
Post: NE Adrenal: epi |
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How is HR increased?
SNS/PNS Receptor Location NT Influence |
SNS RIGHT Side
B1 SA node NE **chronotropicity |
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How is Conduction velocity increased?
SNS/PNS Receptor Location NT Influence |
SNS, RIGHT side
B1 AV Node NE Dromotropicity |
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How is contractility increased?
SNS/PNS Receptor Location NT Influence |
SNS, LEFT side
B1 Vent Myocardium NE Inotropic |
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what N carries PNS?
distinguish R and L branches |
Vagus
R: SA node L: AV node |
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where do post gang parasymp act?
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nodal tissue
conductile tissue **slight atrial myocardium innervation |
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The SA node receives innervation from where (SNS, PNS)
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SNS: Right
PNS: Right |
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The AV node receives innervation from where (SNS, PNS)
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SNS: Right
PNS: Left |
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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 |
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What is an ACh agonist
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atropine, will inhibit Muscarinic (PNS) receptors
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what effect will M2 receptors have on the heart. what division of ANS. What NT
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PNS
ACh Decrease HR (SA) Decrease Conduction (AV) Decreased Contractility |
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Where are B1 and B2 located? what division of ANS
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SNS
B1: Heart, conductile & cantractile B2: Coronary Vascular SM (dilate) |
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what does the a1 receptor do?
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Constricts Vascular SM
NE SNS |
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What receptors have antagonistic effects on Vacular SM
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a1: constrict vascular SM
b2: dilate vascular SM |
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what is the major PNS receptor for cardiac stuff? where is it located, what effect does it have, what receptor has opposite effects
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M2
heart (SA, AV, conctractile?) Decreases, HR, Decreases AV conduction, Decreases contractility ACh B1 in the heart does the opposite |
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what is the most important SNS cardiac receptor subtype. what does it do?
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B1
Increase HR Increase Contractility Increase conduction in AV node NE |
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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 |
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What G protein does SNS activate? PNS?
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SNS: B1, Gs
PNS: M2, Gi |
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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 |
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how is the slope of the pacemaker potential increased
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B1 SNS Increase HR
increases Na conductance (funny current) to increase the rate of depolarization SA node Chronotropicity |
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how is the slope of the pacemaker decreased
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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 |
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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 |
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How is conduction velocity decreased
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Dromotropicity
AV node PNS **decreased Ca conductance, increased K conductance, decreased upstroke, increased PR |
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how is conduction velocity increased
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dromotropicity
AV node SNS **increased rate of doastolic depolarization, decreased PR interval, increased Upstroke (increased Ca conductance), increased PKF conduction |
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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 |
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how is calcium clearance/reuptake increased? what does this do to contractility?
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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 |
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what are the effects of positive inotropicity (SNS) on P when V is constant
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increased pressire
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Ne increases the velocity of mm fiber shortening, what effect does this have on contraction
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increases
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how are SNS PNS related
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both are tonically active, one will win out
**at rest PNS wins |
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what branch of ANS is more active at rest
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PNS
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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 |
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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 |
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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 |
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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 |
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where is a1 located and what is its signal transduction path
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a1: vascular SM, constriction
increase release of Ca from SR, increase Ca influx |
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where is a2 located and what is its signal transduction path
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vascular SM
inhibit adenyly cyclase, decrease cAMP |
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what is the signal transduction path of b1
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B1, in the heart, increase HR, conduction, contractility
increase adenyly cyclase and increase cAMP |
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what is the signal transduction path of b2
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Vascular SM, constriction
activate adenyly cyclase and increase cAMP. also increase cAMP dependent kinase actibity |
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what is the signal transduction path of M2
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M2 in heart, decrease HR, decrease conduction velocity, decrease contractility
**inhibit adenyly cyclase, decrease cAMP **increase k conductance |
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what is the signal transduction path of M3
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cause dilation
**increased intracellular Ca, increased NO production |