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CVS > Autonomic Control Of The CVS > Flashcards

Autonomic Control Of The CVS Flashcards

1
Q

What physiological functions are regulated by the ANS?

A

– Heart rate, BP, body temperature… etc (homeostasis)

– Co-ordinating the body’s response to exercise and stress

– Largely outside voluntary control

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2
Q

What type of tissues does the ANS work on?

A

– smooth muscle (vascular and visceral)

– exocrine secretion

– rate and force of contraction in the heart

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3
Q

What are the two divisions of the ANS?

A
  • Parasympathetic nervous system
  • Sympathetic nervous system
  • This division is based on anatomical grounds (where their pre-ganglion if neurons emerge from the nervous system) not their neurotransmitter

P - Cranial-sacral origin
S- Thoraco-Lumbar origin

• Some text books include a third division the Enteric nervous
system
– Network of neurones surrounding GI tract
– But it is normally controlled via sympathetic and parasympathetic fibres

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4
Q

What effect does the SANS and PANS have on:

1) pupil of eye
2) airways of lungs
3) heart
4) sweat glands

Which receptors are activated in both divisions?

A

1) dilation - alpha 1

Contraction - M3

2) relax - beta 2

Contract - M2

3) Contract harder and faster - Beta 1

Decrease rate - M2

4) Localised secretion (palms) - alpha 1
Generalised secretion - M3

NO effects on PANS

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5
Q

Does the sympathetic system differentials activate the body?

A

YES!!

Sympathetic drive to different tissues is independently regulated

• eg sympathetic activity to the heart can be increased without increasing
activity to GI tract

• on some occasions (fight or flight) there can be a more co-ordinated
sympathetic response

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6
Q

Which part of the cardiovascular system does the ANS control?

A

It controls:

– heart rate

– force of contraction of heart

– peripheral resistance of blood vessels

– Also controls amount of venoconstriction

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7
Q

Which part of the CVS does the ANS not control?

A

The ANS does not initiate electrical activity in the heart. This is done spontaneously by the cells of the pacemaker tissue.

• Denervated heart still beats, but at faster rate
- the Innervation controls the speed to the heart beat

• At rest the heart is normally under vagal influence

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8
Q

What would happen if you denervated the heart?

A

Denervated heart still beats, but at faster rate

Innervation controls the speed and force of contraction, does not initiate it

At rest the heart is normally under vagal influence

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9
Q

Where does the parasympathetic input to the heart come from?

A

• Preganglionic fibres
- 10th (X) cranial nerve
= VAGUS

  • Synapse with postganglionic cells on epicardial surface or within walls of heart at SA and AV node
  • postganglionic cells release ACh

• acts on M2-receptors
– decrease heart rate (-ve chronotropic effect)
– decrease AV node conduction velocity

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10
Q

Where does the sympathetic input to the heart come from?

A

• Postganglionic fibres from the sympathetic trunk

• Innervate SA node, AV node and myocardium
– Release noradrenaline

• Acts mainly on β1
– increases heart rate (+ve chrontropic effect) adrenoreceptors
– AND increases force of contraction (+ve inotropic effect)

• Note: β2 and β3 adrenoreceptors are also resent in the heart, but the main effect is mediated by β1 receptors.

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11
Q

How is the level of parasympathetic and sympathetic outflow controlled?

A

In the brain, the medulla oblongata, there’s a cardiovascular control centre that control the level of parasympathetic and sympathetic outflow

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12
Q

What are baroreceptors? Where are they found in the heart?

A

Receptors that measure pressure

In the heart, they measure arterial blood pressure.

They are found in the arch of the aorta and in the carotid sinus (bulge in carotid artery)

They send inputs to CV centre and say the state of the blood pressure in order to maintain homeostasis of blood pressure

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13
Q

What is the pacemaker potential?

A

The slow depolarisation to threshold before an AP

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14
Q

Describe how the pacemakers of the heart work

A

• Cells in the sinoatrial node (SA node) steadily depolarise toward threshold
– slow depolarising pacemaker potential
– turning on of a slow Na+ conductance (If - funny current)
– opening of Ca2+ channels

• AP firing in the SA node sets the rhythm of the heart

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15
Q

How does the ANS affect the pacemaker potential?

A

Sympathetic activity increases slope - less time between APs

Parasympathetic activity decreases
slope - more time between APs

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16
Q

How does the sympathetic system exert its effects on pacemaker potential?

A
  • sympathetic effect mediated by β1 receptors
  • They are G-protein coupled receptors
  • They are G alpha s and so they stimulate adenylate cyclase enzyme
  • This leads to increase in cAMP in cell
  • This speeds up pacemaker potential because the pacemaker current channels are HCN (hyper polarisation activated cyclic nucleotide gated channels) and cAMP is a cyclic nucleotide
17
Q

How does the parasympathetic system exert its effects on pacemaker potential?

A
  • Parasympathetic effect mediated by M2 receptors
  • These receptors are G alpha i protein coupled receptors, so they are inhibitory
  • It inhibits adenylate cyclase so you get reduced cAMP
  • This causes the pacemaker potential to depolarise more slowly
  • B gamma subunits of G protein receptors acts on K+ channels
  • This increase K+ conductance
  • Cells become more negative and further away from threshold
  • However, because cAMP is decreased, it won’t activate quickly
18
Q

How does noradrenaline increase force of contraction?

A

NA acting on β1 receptors in myocardium causes an increase in cAMP

This activates PKA

PKA then goes on to phosphorylated Ca2+ channels

  1. phosphorylation of Ca2+ channels increases Ca2+ entry during the plateau of the AP
  2. increased uptake of Ca2+ in sarcoplasmic reticulum
  3. increased sensitivity of contractile machinery to Ca2+

• All lead to increased force of contraction

19
Q

What are the ANS effects on vasculature?

A

• Most vessels receive sympathetic innervation
– exceptions
• some specialised tissue eg erectile tissue have parasympathetic innervation

• most arteries and veins have α1-adrenoreceptors
– coronary and skeletal muscle vasculature also have β2 receptors

20
Q

What is the importance of vasomotor tone?

A

It allows for vasodilation and vasoconstriction

If the sympathetic output is decreased = vasodilation

Normal = vasomotor tone

Increased = Vasoconstriction

21
Q

Some blood vessels have β2 adrenoceptors as well as alpha 1 adrenoceptors, which ones?

When are they used?

A

Skeletal muscle
Liver
Myocardium

  • Noradrenaline released from SNS will largely activate the Alpha 1 adreno receptors
  • Circulating adrenaline has a higher affinity for β2 adrenoceptors than for α1 receptors
  • At normal physiological concentration circulating adrenaline will preferentially bind to β2 adrenoceptors
  • At higher concentrations it will also activate α1 receptors
22
Q

What are the effects of b2 and a1 adrenoreceptors on VSM?

A

• Activating β2 adrenoreceptors cause vasodilation
– increases cAMP –> PKA –> opens potassium channels + inhibits MLCK –> relaxation of smooth muscle

• Activating α1 adrenoreceptors causes vasoconstriction

  • Stimluates IP3 production
  • Increase in intracellular Ca2+ from stores and via influx of extracellular Ca2+ –> contraction of smooth muscles
23
Q

What is the role of local metabolites?

A

This is the main thing that increases blood flow to tissues

The more active the tissue gets, the more they will produce metabolise
- e.g. adenosine, K+, H+, increase PCO2

Local increases in metabolites have a strong vasodilator effect

Metabolites are more important for ensuring adequate perfusion
of skeletal and coronary muscle than activation of β2-receptors

24
Q

How is CVS pressure controlled by the brain?

A

• Changes in the state of
the system are communicated to the brain via afferent nerves

– Baroreceptors (high
pressure side of system)

– Atrial receptors (low
pressure side of system - venous pressure and how much the heart fills)

• Alters activity of efferent
nerves

25
Q

What are baroreceptors?

How do they work?

A

Nerve endings in the carotid sinus and aortic arch that are sensitive to stretch.

They are important for maintaining blood pressure

They have afferent flow to the CVS control centre in the medulla in the brain. This centre monitors how much sympathetic and parasympathetic outflow is needed

Increased arterial pressure stretches these receptors.

If mean arterial pressure increases, the baroreceptors will be activated, travel to the afferent pathways along vagus nerve and glossopharyngeal nerve eventually the towards the CVS control centre in the medulla.

This will detect increase firing and will reduce sympathetic outflow to the heart.

This means that heart rate and construction of vessels are reduced, the arterial pressure will reduce as a result

As a result, you will increase the parasympathetic outflow to the heart.

The balance of sympathetic and parasympathetic outflow will change depending on whether arterial pressure increases or decreases

26
Q

Why is the baroreceptors reflex so important? Give an example of when it is important.

A
  • The baroreceptor reflex is important for maintaining blood pressure over short term - acute changes
  • It compensates for moment to moment changes in arterial BP

For example, if lying down and then immediately stand up, you get a redistribution of blood to body - more blood to legs.

This will cause drop in arterial pressure and body has to respond to that because arterial pressure must be maintained so ensure brain is properly perfused

Otherwise you’ll feel light-headed and dizzy

This is also important during exercise

  • metabolites will cause vasodilation
  • sympathetic outflow to cause vasodilation too

• HOWEVER…. Baroreceptors can re-set to higher levels with persistent increases in blood pressure

  • this means it will operate at higher pressure and that’s how you get hypertension
27
Q

What are sympathomimetics?

A

A group of drugs that act on the ANS by mimicking the sympathetic nervous system

28
Q

When are sympathomimetics used?

A

• cardiovascular uses
– administration of adrenaline to restore function in cardiac arrest - it works via vasoconstriction by acting on alpha 1 receptors

–β1 agonist - dobutamine may be given in cardiogenic shock (pump failure)

– adrenaline administered for anaphylactic shock

• other uses
–β2 agonist – salbutamol for treatment of asthma

29
Q

What are adrenoreceptor antagonists and when are they used?

A

They are a group of drugs that antagonise or oppose the effects of molecules acting on adreno receptors

• α1-adrenoreceptor antagonists
- alpha 1 antagonists eg prazosin
– anti-hypertensive agent – but there are better things to use

  • Would only be used with resistant hypertension
  • inhibits NA action on vascular smooth muscle α1 receptors - vasodilation

• β-adrenoreceptor antagonists
– propranolol
• non-selective β-antagonist
• slows heart rate and reduces force of contraction (β1) but also acts on bronchial smooth smooth (β2) - bronchoconstriction

– atenolol
• selective β1 (cardio-selective) - less risk of bronchoconstriction and side effects as its specific

30
Q

What are cholingerics? And what are they used for?

A

Cholinergics are muscadine agonists and antagonists

• Muscarinic agonists
– e.g. pilocarpine 
– used in treatment of glaucoma
- activates constrictor pupillae
muscle 
- This opens the Canal of Schlemm so that the fluid can be drained 
• Muscarinic antagonists
– e.g. atropine or tropicamide
– increases heart rate, bronchial
dilation 
– used to dilate pupils for
examination of the eye

CVS (11 decks)

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