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SA Cardiovascular system > S4) The Autonomic Nervous System > Flashcards

S4) The Autonomic Nervous System Flashcards

1
Q

What does the autonomic nervous system do?

A

Regulates physiological functions

  • Heart rate
  • BP
  • Body temperature
  • coordinates bodys response to exercise and stress
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2
Q

Describe two general ways in which the ANS can regulate physiological functions

A
  • Sympathetic activity is increased under stress
  • Parasympathetic activity is increased under basal conditions
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3
Q

What does the ANS exert control over?

A
  • Smooth muscle
  • Exocrine secretion
  • Inotropy (increased contraction) & chronotropy (increased heart rate) in heart
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4
Q

Describe the neurotransmitters and receptors acting on the heart in the parasympathetic nervous system and sympathetic nervous system respectively

A
  • PNS action on heart rate is mediated via acetylcholine acting on M2 muscarinic receptors
  • SNS action on heart rate and contractility is mediated via noradrenaline acting on β1 adrenoreceptors
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5
Q

Outline the ANS control of the cardiovascular system

A

The ANS controls:

  • Heart rate
  • Force of contraction of heart
  • Peripheral resistance of blood vessels
  • Amount of venoconstriction
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6
Q

In 4 steps, describe the parasympathetic input to the heart

A

⇒ Preganglionic fibres via vagus nerve

⇒ Synapse with postganglionic cells on epicardial surface / within heart wall of at SAN/AVN

⇒ Postganglionic cells release ACh

⇒ ACh acts on M2 receptors ( G coupled protein receptors)

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7
Q

What is the effect of the PNS on the heart?

A
  • Decrease heart rate (negative chronotropic effect)
  • Decrease AVN conduction velocity
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8
Q

In 4 steps, describe the sympathetic input to the heart

A

⇒ Postganglionic fibres from the sympathetic trunk

⇒ Innervate SAN, AVN and myocardium

⇒ NA is released

⇒ NA mainly on β1 adrenoreceptors

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9
Q

What is the effect of the SNS on the heart?

A
  • Increases heart rate (positive chronotropic effect)
  • Increases force of contraction (positive inotropic effect)
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10
Q

Outline the opposing sympathetic and parasympathetic effects on pacemaker potentials

A
  • Sympathetic activity:

I. Mediated by β1 receptors

II. GPCRs increase cAMP which speeds up the pacemaker potential

  • Parasympathetic activity:

I. Mediated by M2 receptors

II. GPCRs increase K+ conductance and decrease cAMP

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11
Q

In 4 steps, explain how noradrenaline increases the force of contraction

A

NA acts on β1 receptors in myocardium:

⇒ Increased cAMP activates PKA (protein kinase)

⇒ Phosphorylation of Ca2+ channels increases Ca2+ entry

⇒ Increased uptake of Ca2+ in SR

⇒ Increased sensitivity of contractile machinery to Ca2+

=> more contraction

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12
Q

What type of receptors are found in the systemic vasculature?

A
  • Most blood vessels have α1-adrenoreceptors
  • Some blood vessels have β2-adrenoreceptors e.g. myocardium, liver, skeletal muscle vasculature
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13
Q

Describe the effects of increased/decreased sympathetic output to the peripheral vasculature

A
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14
Q

Describe the effect of circulating adrenaline on blood vessels which have both β2 adrenoceptors and α1 adrenoreceptors

A

Circulating adrenaline has a higher affinity for β2 adrenoceptors than for α1 receptors:

  • At [physiological], it will preferentially bind to β2 adrenoceptors
  • At [higher], it will also activate α1 adrenoreceptors
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15
Q

Describe the opposing effects of β2 and α1 adrenoreceptors on vascular smooth muscle

A
  • Activating β2 adrenoreceptors causes vasodilation:

I. Increases cAMP → Opens K+ channels & inhibits MLCK

II. Relaxation of smooth muscle

  • Activating α1 adrenoreceptors causes vasoconstriction:

I. Stimulates IP3 production → increase [Ca2+]i

II. Contraction of smooth muscle

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16
Q

Describe the cardiovascular control system established by the ANS in terms of afferent and efferent nerves

A
  • Changes are communicated to the brain via afferent nerves:

I. Baroreceptors (high pressure side of system)

II. Atrial receptors (low pressure side of system)

  • Alters activity of efferent nerves
17
Q

What are baroreceptors and what do they do?

A
  • Baroreceptors are nerve endings in the carotid sinus and aortic arch are sensitive to stretch
  • Increased arterial pressure stretches these receptors
18
Q

Briefly, outline the baroreceptor reflex

A

. - maintains blood pressure over a short time

  • re-set to higher levels with persistent increase in blood pressure
19
Q

What are the three types of drugs which act on the ANS?

A
  • Sympathomimetics
  • Adrenoceptor antagonists
  • Cholinergics - mimic action of acetyl choline
20
Q

What are the two types of sympathomimetics?

A
  • α-adrenoceptor agonists
  • β-adrenoceptor agonists
21
Q

Describe the uses of sympathomimetics

A
  • Adrenaline to restore function in cardiac arrest/anaphylactic shock
  • β1 agonists given in cardiogenic shock (pump failure)
  • β2 agonists used for treatment of asthma
  • administer adrenaline to restore function and support
22
Q

What are the two types of adrenoreceptor antagonists?

A
  • α-adrenoreceptor antagonists (vasodialation)
  • β-adrenoreceptor antagonists (bronchoconstirction)
23
Q

Describe the uses of adrenoreceptor antagonists

A
  • α-adrenoreceptor antagonists – inhibits NA action on vascular smooth muscle α1 receptors, causing vasodilation
  • β-adrenoreceptor antagonists – slows HR, reduces force of contraction (β1) and causes bronchoconstriction (β2)
24
Q

What are the two types of cholinergics?

A
  • Muscarinic agonists
  • Muscarinic antagonists
25
Q

arrangment of pre and post ganglionic neurones in sympathetic and parasympathetic neurones

A

sympathetic

  • Small preganglionic
  • long postganglionic

parasympathetic

  • long preganglionic
  • short post ganglionic

all attach by a nictotinic acetylcoA receptor

26
Q

pacemaker of the heart

A

cells in SA steadily depolarise towards threashold

  • slow depolarising pacemaker potential
  • turning on of a slow Na conductance (funy current)
  • opening of some Ca channels
  • turning off K conductance
27
Q

examples of ANS control

A
28
Q

sympathetic activity causing venoconstriciction

A

increases venous pressure = more blood returned

29
Q

what does thr ANS not do

A
  • does not inittate electrical activity as its spontaneously actuve due to pacemaker cells
  • when heart is denervated heart still beats but much faster ==> shows the parasympathetic has an effect on heart via vagus nerve
30
Q

effect of ANS on pacemaker cells

A
31
Q

role of metabolites

A
  • main cause of vasodialation
  • produced in active tissue
32
Q

sympathetic output on vasodialation

A

want vasoconstriction for increased venouse return

33
Q

effects of B2 and A1 adenoreceptors on smooth muscle

A
  • activating B2 adenoreceptors = vasodialation

(^CAMP ^PKA ^K channels inhibits MLCK (allows contraction) = relaxation)

  • noradrenaline activating a1 = vasoconstriction

(^IP3 production, ^influx of extracellular Ca, Ca binds to caM, activates MLCK, phosphorylates myosin light chain, ^ contraction of smooth muscle)

34
Q

3 types of G coupled protein receptors

A

alpha (Q, I - inhibits CAMP, S - stimulates CAMP)

beta

gamma

35
Q

receptors

A

B1 = sympathetic = increase contraction = agonist given in a cardiogenic shock
M2 = parasympathetic
a1 adrenoreceptors = vasoconstriction
B2 adrenoreceptors = adrenaline has more affinity than a1 = vasodilation = asthma

SA Cardiovascular system (16 decks)

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