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Cardiovascular system > Lecture 10- Autonomic cardiac control > Flashcards

Lecture 10- Autonomic cardiac control Flashcards

1
Q

The ANS has important for regulating many physiological functions inc…

A

HR, BP, body temp etc (homeostasis)

Fight or flight response (stress response)

*Outside voluntary control*

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2
Q

ANS control over specific tissue

A

Smooth muscle

Exocrine secretion

Rate and force of contraction in the heart

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3
Q

Two divisions (defined by their origin- anatomical grounds)

A

Parasympathetic- craniosacral origin

Sympathetic- thoracolumbar origin

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4
Q

sympathetic neurones

A

preganglionic within CNS (short), postganglionic innervates target tissue (long)

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5
Q

parasympathetic neurones

A

preganglionic (long), post ganglionic neurone are within the target tissue (short)

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6
Q

function of the ANS

A

Where parasympathetic and sympathetic divisions both innervate a tissue they often have opposite effects

  • Sympathetic activity is increased under stress
  • Parasympathetic system is more dominant under basal conditions
    • Both work together to maintain balance
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7
Q

sympathetic effect and receptor: pupil of the eye

A

dilation (contracts raidal muscle)

alpha1

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8
Q

sympathetic effect and receptor: airways of lungs

A

relax

Beta1

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9
Q

sympathetic effect and receptor: heart

A

increase rate (chronotropy) and force of contraction (inotropy)

Beta1

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10
Q

sympathetic effect and receptor: sweatglands

A

localised secretion (e.g. palms)–> alpha1

generalised secretion–> M3

*Sweat glands- one of the only sympathetic receptors that use ACh*

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11
Q

parasympathetic effect and receptor: pupil of eye

A

contraction (contracts sphincter muscle)

M3

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12
Q

parasympathetic effect and receptor: airways of lungs

A

contracts

M3

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13
Q

parasympathetic effect and receptor: heart

A

decrease rate

M2

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14
Q

parasympathetic effect and receptor: sweat glands

A

no effeect

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15
Q

ANS control of CVS

A

Heart rate

Force of contraction of heart

Peripheral resistance of blood vessels

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16
Q

what does thr ANS not do to the CVS

A

Initiate electrical activity in the heart

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17
Q

if the heart was dennervated

A

Dennervated heart still beats, but at a faster rate

At rest the heart is normally under vagal (parasympathetic) influence

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18
Q

(1) Parasympathetic input of the heart

A
  • Preganglionic fibres- 10th X cranial nerve VAGUS
  • Synapse with postganglionic cells on epicardial surface or within the walls of the heart at the SA and AV node
    • Slow conduction at both SA and AV
  • Post ganglionic release ACh
    • Acts on M2 receptors
    • Decrease heart rate (-ve chronotropic effect)
    • Decrease AV node conduction velocity
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19
Q

(2) Sympathetic input to the heart

A
  • Post ganglionic fibres from the sympathetic trunk
  • Innervates SA, AV node and myocardium
    • Release noradrenaline
  • Acts mainly on B1 adrenoreceptors
    • Increases heart rate (+ve chronotropic effect)
    • And increases forces of contraction (+ve inotropic effect)
    • B2 and B3 also present in heart, but the main effect is mediated by B1 receptors
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20
Q

autonomic NS input into the heart diagram

A
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21
Q

The pacemaker of the heart

A

Cells in the SAN steadily depolarise towards threshold

  • Slow depolarising pacemaker potential
  • Turning on of a slow Na+ conductance-HCN (If-funny current)
  • Opening of ca2+ channels
  • AP firing in the SA node set the rhythm of the heart
22
Q

Effects of ANS on the pacemaker potential (chronotropic): sympathetic

A

effects mediated by b1 receptor

GPCR

  1. increase cAMP
  2. speed up pacemaker potential

HCN – cyclic nucleotide gated

–>Increase cAMP, increase If current

23
Q

Effects of ANS on the pacemaker potential: parasympathetic

A

effects mediated by M2 receptors

GPCR

  1. increased K+ conductance
  2. decrease CAMP
24
Q

How does NA increase force of contraction? (inotropic)

A
  • NA acting on B1 receptors in myocardium causes an increase in cAMP –> activates PKA (GalphaS)
    • Phosphorylation of Ca2+ channels increase Ca2+ entry during the plateau of the AP
    • Increase uptake of Ca2+ in SR
    • Leads to increased force of contraction
25
Q

ANS effects on vasculature

A

Most vessels receive sympathetic innervation (bar erectile tissue which does have some parasympathetic innervation)

26
Q

which receptors do most arteries and veins have

A
  • Most arteries and veins have alpha1-adrenoreceptors
  • Coronary and skeletal muscle vasculature also have B2- receptors
27
Q

Vasomotor tone allows for dilation to occur

A

Have to have some basal level of vascular tone to make sure the vessels have somewhere to dilate

i. e. the less sympathetic outcome –> vasodilation
e. g. to reduce BP–> dilate vessels

28
Q

which blood vessels have B2 adrenoreceptors as well as alpha1 adrenoreceptors

A

e.g. skeletal muscle, myocardium and liver

29
Q

why do skeletal muscle, myocardium and the liver have B2 and alpha1 adrenoreceptors

A
  • NA released from SNS will bind to alpha 1 will causes vasoconstriction
  • Circulating adrenaline preferentially acts on B2 receptors (will also act on alpha1 as conc gets higher)
  • At physiological conc will activate B2–> vasodilation
  • If you increase conc of circ adrenaline, then at higher conc it will work on alpha1 –> causing vasoconstriction
30
Q

Effects of B2 adrenoreceptors on vascular smooth muscle

A

Activating B2 adrenoreceptors causes vasodilation

  1. Increases cAMP
  2. Activates PKA
  3. opens potassium channels and inhibits MLCK
  4. relaxation of smooth muscle
31
Q

Effects of alpha1 adrenoreceptors on vascular smooth muscle

A

Activating alpha1 adrenoreceptors causes vasoconstriction

  1. Stimulates IP3 production
  2. Increase in (Calcium) in from stores and via influx of extracellular Ca2+
  3. contraction of smooth muscle
32
Q

local metabolites which cause vasodilation

A
  • Adenosine
  • K+
  • H+
  • Increased PCO2
  • Locale increase in metabolites have strong vasodilator effects
33
Q

local metabolists are more important for ensuring

A

adequate perfusion of skeletal and coronary muscle than activation of B2 receptors

34
Q

Changes in the state of the cardiovascular system are communicated to the brain via

A

afferent nerves:

  • Baroreceptors (high pressure side of system)
  • Atrial receptors (low pressure side of the system)

will alter activity of efferent nerve

35
Q

baroreceptor nerve endings found in…. and are sensitive to ….

A

carotid sinus and aortic arch sensitive to stretch

36
Q

baroreceptors during an increased BP

A
  1. Increased arterial pressure stretches these receptors
  2. Afferent nerves report back to medullary centre
  3. Parasympathetic nervous system activated
    • Vasodilation of vessels
    • Reduced inotropy of the heart
37
Q

baroreceptor reflex

A
  • Important for maintaining blood pressure over short term
  • It compensates for moment to moment changes in aBP
  • However Baroreceptors can re-set to higher levels with persistent increases in blood pressure
38
Q

drugs which act on the ANS

A
  1. Sympathomimetics
    • Alpha-adrenoreceptors agonists
    • B-adrenoreceptor agonists
  2. Adrenoreceptor antagonists
  3. Cholinergics
    • Muscarinic agonists and antagonists
39
Q

name some sympathomimetics

A

adrenaline, dobutamine and salbutamol

40
Q

Admin of adrenaline

A

to restore function in cardiac arrest

41
Q

dobutamine is a

A

B1 agonist that may be given in cardiogenic shock (pump failure)

42
Q

adrenaline also administed for

A

anaphylactic shock

43
Q

salbutamol is a

A

B2 agonist- treatment for asthma

44
Q

adrenoreceptor agonists

A

Alpha-adrenoreceptors antagonists

B-adrenoreceptor antagonists

45
Q

Alpha-adrenoreceptors antagonists

A

Alpha 1 antagonist e.g. prazosin

  • Anti-hypertensive agent
  • Inhibits NA action on vascular smooth muscle alpha 1 receptors- vasodilation
46
Q

B-adrenoreceptor antagonists

A

propanol

atenolol

47
Q

Propranolol

A
  • Non-selective B1/B2 antagonists
  • Slows heart rate and reduces force of contraction (B1) but also acts on bronchial smooth muscle (B2)- bronchoconstriction
48
Q

Atenolol

A

Selective B1 (cardio-selective)- less risk of bronchoconstriction

49
Q

cholinergics

A

muscarininc agonists

muscarinic antagonists

50
Q

muscarininc agonists

A

e. g. pilocarpine- used in treatment of glaucoma
* activates constrictor pupillae muscle

51
Q

Muscarinic antagonists

A

e.g. atropine or tropicamide

  • Increases heart rate, bronchial dilation
  • Used to dilate pupils for examination of the eye

Cardiovascular system (30 decks)

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