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Cardiovascular (F&F) > Autonomic NS & Cardiovascular system > Flashcards

Autonomic NS & Cardiovascular system Flashcards

1
Q

Autonomic nervous system

A

-consists of parasympathetic (vagal) and sympathetic branches or divisions
-supplies most organs including heart, blood vessels, kidneys/adrenal glands

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2
Q

Autonomic control concerning cardiovascular system

A

-blood pressure (heart rate/contractility, blood volume, vascular tone)
-water and electrolyte balance, and urination that impact blood volume

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3
Q

Where do inputs converge in the brain?

A

-medullary centers
-location for both sympathetic and parasympathetic/vagal control. When one is increased, the other decreases (push and pull)

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4
Q

Parasympathetic nervous system

A

-rest and digest
-ganglia located away from spine (in organ)
-more specific targets (no chain ganglia/no need to target all organs)

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5
Q

Nerves of parasympathetic nervous system

A

-project from cranial and sacral nerves

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6
Q

Parasympathetic nerve of the heart

A

-Vagus nerve (X) directly innervates the heart
**triggers tonic firing in heart, slows down heart

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7
Q

Signalling and receptors of parasympathetic

A

-Cholinergic (acetylcholine)
-nicotinic and muscarinic receptor signalling

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8
Q

Sympathetic nervous system

A

-fight or flight
-ganglia located near the spine (post ganglionic nerve from sympathetic chain)
-not targeted (chain ganglia response/effects all organs)
-tonic firing (sustained response)

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9
Q

What do sympathetic nerves innervate?

A

-heart
-arteries
-veins
-adrenal glands

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10
Q

Signalling and receptors of sympathetic nervous system

A

-cholinergic signalling at ganglia (acetylcholine) at nicotinic receptors
-adrenergic signalling (NE and Epi) at organs at alpha and beta adrenergic receptors
-neurohumoral signaling at adrenal glands

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11
Q

Acetylcholine on muscarinic receptors

A

-In heart: decreased heart rate, stoke volume, cardiac output
-In arterioles: decreased vasoconstriction (**not parasympathetic control/nerves involved in NT release)

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12
Q

Acetylcholine on nicotinic receptors

A

-In ganglia: stimulates post-ganglionic nerves in both parasympathetic and sympathetic nervous system resulting in INCREASED BP

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13
Q

Preganglionic nerve

A

-arise from brain stem
-synapse on autonomic ganglia
-always rely on cholinergic (acetylcholine) and nicotinic receptors

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14
Q

Postganglionic nerve

A

-arise from autonomic ganglia
-synapse at end organ
-varying neurotransmitters and receptors depending on whether parasympathetic and sympathetic

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15
Q

Ganglionic transmitters

A

-relay signal between pre and post ganglionic nerves

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16
Q

Postganglionic transmitters

A

-relay signal to end organ

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17
Q

Parasympathetic nervous system signalling

A

-post ganglionic nerve relies on cholinergic (acetylcholine) release from autonomic ganglia and muscarinic receptors on organs (and nicotinic in autonomic ganglia which activates post ganglionic fiber and muscarinic receptors)

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18
Q

Sympathetic nervous system signalling

A

-post ganglionic nerve synapse on chain ganglia, and rely on the release of adrenergic (norepinephrine or epinephrine) and binding at alpha and beta adrenergic receptors

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19
Q

Competition of parasympathetic and sympathetic nervous system

A

-inputs from either side are always competing
-when one increases, the other decreases (push-pull mechanism)

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20
Q

Parasympathetic innervation of heart

A

-vagus nerve innervates the SA and AV nodes of heart

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21
Q

Sympathetic innervation of heart

A

-innervate the SA and AV nodes, and the ventricular myocardium

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22
Q

How does the nervous system slow down the heart?

A

-Action potential of the heart is generated at the node with the highest frequency (SA and AV nodes)
-To slow down the heart, need to reduce the frequency and conduction of AP at both the SA and AV nodes
**muscular components (contractility and relaxation) are modulated by adrenergic (sympathetic) vs. vagal (parasympathetic) nerves

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23
Q

Cholinergic off signal (parasympathetic)

A

-the recycling of acetylcholine by acetylcholinesterase into choline and acetate tells system to turn off production of acetylcholine

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24
Q

Parasympathetic-cholinergic/acetylcholine acting on SA nodes

A
  • Acetylcholine binds to muscarinic receptors
  • Coupled with K channels and T-type calcium channels (increases K, decreases Ca)
  • Reduced cAMP
  • Results in drawn out duration of AP and slowed down heart rate
    **active at rest, mostly withdrawn during stress
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25
Q

What does vagal innervation/activation of the heart do?

A

-decreases chronotropy (rate of firing
-decreases dromotropy ( conduction of heart)
**decreases CO, MAP

26
Q

Signs of overactivation of parasympathetic nervous system

A

-diarrhea
-straining
-colic
-shortness of breath
-twitching (nicotinic)
-salivation
-constricted pupils
-depressed heart rate

27
Q

Horse ingested carbamates (cholinesterase inhibitor)

A

-turns off acetylcholinesterase, which results in no off signal and large presence of acetylcholine
-lots of acetylcholine means that the muscarinic receptors are saturated and causing a constant decrease in heart rate AND nicotinic receptors are saturated causing muscles to fire resulting in muscle twitching

28
Q

Drugs affecting vagal innervation/cholinergic

A

-cholinergic drugs/cholinesterase inhibitors

29
Q

Adrenergic off signal (sympathetic)

A

-Tyrosine converted to dopamine, then norepinephrine
-Breakdown of norepinephrine into metabolites is NOT an off signal
-Instead norepinephrine binds to alpha 2 adrenergic receptors on post ganglionic nerve. This is the negative feedback loop and turns off norepinephrine production

30
Q

Sympathetic- adrenergic/norepinephrine acting on SA nodes

A

-norepinephrine binds to beta 1 adrenergic receptors
-activates adenylate cyclase and cAMP
-turns on protein kinase A
-Protein kinase A activated Na funny channels and T-type Ca channels (increase Na and Ca entry). Also works on L-type Ca channels in cardiomyocytes, increasing heart rate
**modestly active at rest, engaged during stress

31
Q

Norepinephrine acting on Heart

A

-increases chronotropy (rate of firing)
-increases dromotropy (rate of conduction)
-increases inotropy (contractility)
-increases lusitropy (speeds relaxation)
**increases CO and MAP

32
Q

Drugs affecting adrenergic innervation

A

-beta blockers class of drugs
-sympatholytic drugs

33
Q

Parasympathetic Nervous System control

A

-does not have a main role in systemic vasomotor control

34
Q

Epinephrine vs. norepinephrine production

A

-Epi= 80%
-NE=20%
**preferential release of epinephrine over norepinephrine

35
Q

Adrenergic nerve innervation

A

-innervates both arteries and veins
*NE acts on alpha1-adrenergic receptors

36
Q

Sympathetic activation of adrenals

A

-stimulates the release of NE and Epi
-split is 80-20; favours Epi

37
Q

What does Epi and NE bind to?

A

-Epi acts on beta2 adrenergic receptors (and alpha1,beta1)
-NE acts on alpha1-adrenergic receptors (beta1)

38
Q

NE binding and effects

A

-binds to alpha 1 adrenergic= increases vasoconstriction in arteries
-binds to beta1 adrenergic= increases heart rate, stroke volume, cardiac output in Heart

39
Q

Epi binding and effects

A

-binds to alpha 1 adrenergic= increases vasoconstriction in arteries
-binds to beta1 adrenergic= increases heart rate, stroke volume, cardiac output in Heart
-binds to beta2 adrenergic= vasodilation in skeletal muscle vascular beds (arterioles)

40
Q

Alpha 1 adrenergic receptors

A

-NE released from adrenergic nerves (sympathetic) or adrenals (20%)
-alpha 1 receptors located in arteries and veins
-Activation activates the IP3 pathway

41
Q

IP3 pathway

A

-activated by g-coupled alpha1 receptors
-increases intracellular Ca and causes vasoconstriction in arterial and venous side

42
Q

Alpha 1, IP3, activation on arterial side

A

-increased vasoconstriction on arterial side
-increases tone, vascular resistance, and MAP

43
Q

Alpha 1, IP3, activation on venous side

A

-increased vasoconstriction on venous side
-increases tone, venous pressure, venous return
»therefore increasing preload, contractility, cardiac output and MAP

44
Q

Beta 2 adrenergic receptors

A

-Sympathetic activation of adrenals stimulates the release of Epi (80%) and NE (20%)
-both bind to beta 2 adrenergic in the arteries activating the cAMP pathway

45
Q

cAMP pathway

A

-activated by beta 2 adrenergic (mostly Epi, some NE)
-inhibits MLCK, causes dilation on arterial side

46
Q

Beta2 adrenergic, cAMP pathway, activation on arterial side

A

-causes dilation
-decreases tone, vascular resistance, MAP

47
Q

NE and Epi competition

A

Epi preferentially binds to beta2, NE preferentially binds to alpha1
-Epi will cause dilation, NE causes constriction
-NE increases CO and MAP, EPI decreases MAP
***Eventually Epi will saturate all beta2, and will switch to alpha1

48
Q

Nicotinic

A

-in autonomic ganglia, activates postganglionic nerves (PNS/SNS)

49
Q

Muscarinic

A

-in heart, decreases HR

50
Q

Beta1

A

-in heart, increases HR and contractility

51
Q

Beta2

A

-in heart and blood vessels, increases HR, contractility and vasodilation

52
Q

Alpha1

A

-in blood vessels, causes vasoconstriction

53
Q

Alpha2

A

-in blood vessels and preganglionic nerve terminal
-causes vasoconstriction and decreases NE release from nerve terminal

54
Q

What receptors cause increased CO?

A

-Adrenergic/NE at heart and adrenal release of EPI (when high concentration)
-adrenergic/NE on veins, increases preload, leading to increase in CO

55
Q

What receptors cause increased systemic vascular resistance?

A

-Adrenergic/NE on arteries, causes vasoconstriction

56
Q

Baroreceptors

A

-detect stretch
-increased stretch=increased activation of vagal/parasympathetic
-decreased stretch=stops activation of vagal; lifts break on sympathetic

57
Q

Baroreceptor location

A

-located in aortic bodies and carotid bodies

58
Q

Path from baroreceptors

A

-stretch detected by baroreceptors
-information passed to brain via cranial nerves IX and X
-Medullary centers activate either sympathetic or parasympathetic NS

59
Q

Decrease in pressure and baroreceptor result

A

-decrease in pressure
-decrease in baroreceptor firing; leads to brake being lifted and increase in sympathetic NS
-increase in NE, vasoconstriction in vessels, AND increase in heart rate, contractility and CO
-All leads to increase in MAP

60
Q

Increase in pressure and baroreceptor result

A

-increase in pressure, increase in baroreceptor firing
-increase in parasympathetic NS
-acetylcholine acting on muscarinic in heart= decreased HR, SV, and CO
-acetylcholine acting on muscarinic in arterioles= decreased vasoconstriction
-All leads to overall decrease in MAP

61
Q

Using Epi (pharmacology)

A

-MAP does not change much
-pulse pressure increases dramatically and heart rate increases

62
Q

Using NE (pharmacology)

A

-MAP increases
-Pulse pressure increases and heart rate decreases
>increase in pressure, increase in baroreceptors, increase in parasympathetic/decrease in sympathetic= depressing heart rate
-increases tone and increases resistance so would not want to use on animal with very low blood pressure

Cardiovascular (F&F) (19 decks)

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