Autonomic Control Of CVS

Question 1

Where does the majority of the parasympathetic nervous system stem from?

Answer 1

The cranial and sacral regions

Question 2

Where does the majority of the sympathetic nervous system stem from?

Answer 2

Thoracic and lumbar regions

Question 3

What does the ANS control in the CV system?

Answer 3

• heart rate
• force of contraction (inotropy)
• peripheral resistance of blood vessels
• controls amount of venoconstriction

*does not initiate heart beat, only speed and force of beat. (Denervated hearts still beat but at a faster rate~100bpm)

Question 4

How is the parasympathetic NS connected with the heart?

Answer 4

Preganglionic fibres-The vagus nerve (10th cranial nerve)

Post ganglionic cells- epicardial surface/within walls of heart at SA and AV node

Question 5

What neurotransmitter is released by the post ganglionic cells in the parasympathetic NS innervation the heart? What does this act upon?

Answer 5

ACh

Acts on M2-receptors

Question 6

What effects can the parasympathetic NS have on the heart?

Answer 6

Decreased heart rate (-ive chronotropic effect)

Decrease AV node conduction velocity

Question 7

How is the sympathetic NS connected with the heart?

Answer 7

Post ganglionic fibres from the sympathetic trunk

Innervates the SA node, AV node and myocardium.

Question 8

What neurotransmitter is released by the post ganglionic cells in the sympathetic NS innervation the heart? What does this act upon?

Answer 8

Noradrenline

Acts on beta1 adrenoreceptors

**beta 2 and 3 adrenoreceptors are also present in the heart but the main effect is mediated by beta 1 receptors

Question 9

What effects can the sympathetic NS have on the heart?

Answer 9

Increases heart rate (+ive chronotropic effect)

Increases force of contraction (+ive inotropic effect)

Question 10

What part of the brain controls the cv system?

Answer 10

Medulla oblongata

Question 11

How does the body know how to adapt the messages it sends to heart?

Answer 11

It receives information from the baroreceptors in the carotid sinus and the arch of aorta (these measure blood pressure)

And atrial receptors on the low pressure side of system

Question 12

Along what nerve does the information collected by the baroreceptors travel?

Answer 12

Glossopharyngeal nerve (cranial nerve IX)

Sensory nerve

Question 13

What are the two motor (efferent) neurones that innervate the heart?

Answer 13

Vagus (parasympathetic)

Cardiac accelerator nerve (sympathetic)

Question 14

What are the effects of ANS on pacemaker action potentials in the heart?

Answer 14

Sympathetic activity increased the slope (depolarisation occurs quicker) and in the AV node conduction is speed up

Parasympathetic activity decreases slope (depolarisation occurs slower) and in the AV node conduction is slowed

Question 15

By what mechanism does the sympathetic NS increase the speed of pacemaker cells?

Answer 15

Sympathetic effect mediated by beta 1 adrenoreceptors
G-alpha-s (gpcr) increase cAMP which has effect f speeding up pacemaker potentials

*the cAMP can have a direct effect on the enhancement of currents

Question 16

By what mechanism does the parasympathetic NS decrease the activity of the pacemaker cells?

Answer 16

Parasympathetic effect mediated by M2 receptors. G-alpha-i (GPCR) increase k+ conductance and decrease cAMP. Beta-gamma subunit act on k+ channels, meaning the m.p is further from the threshold and it therefore takes longer to fire an AP

Question 17

How does noradrenaline increase force of contraction?

Answer 17

1. It acts on B1 receptors in myocardium which causes an increase in cAMP which in turn activates PKA.
2. Phosphorylation of Ca2+ channels increases Ca2+ entry during plateau of the AP
3. Increased uptake of Ca2+ in SR
4. Increased sensitivity of contractile machinery to Ca2+

All leads to increased force of contraction

Question 18

What type of receptors do most veins and arteries have and what type of innervation do they receive?

Answer 18

A1 adrenoreceptors

Sympathetic

**coronary and skeletal muscle vasculature may also have B2 receptors

Question 19

How is vasodilation controlled?

Answer 19

By turning sympathetic control up and down (there is no parasympathetic innervation)

For vasodilation- stop stimulation
For vasomotor tone- normal stimulation
For vasoconstriction- increase stimulation

All about activation of the A1 adrenoreceptors

Question 20

Some vessels have B2 adrenoreceptors as well as A1 adrenoreceptors. What neurotransmitters are they most sensitive to?

Answer 20

A1- noradrenaline from SNS

B2- more sensitive to circulating adrenaline (as circulating adrenaline has a higher affinity for beta 2 adrenoreceptors)

*at higher concentrations circulating adrenaline will also bind to a1 receptors

Question 21

For those vessels that have both b2 and a1 adrenoreceptors how is vasomotor tone controlled?

Answer 21

For vasodilation- activate b2 adrenoreceptors

For vasoconstriction- activate a1 adrenoreceptors

Question 22

How does activating b2 adrenoreceptors in the vascular smooth muscles cause vasodilation?

Answer 22

Increases cAMP= PKA= opens k+ channels (hyperpolarisation occurs)+ inhibits MLCK (stops phosphorylation of myosin light chain) = relaxation of smooth muscle

Question 23

How does activating a1 adrenoreceptors in the vascular smooth muscles cause vasoconstriction?

Answer 23

Stimulates IP3 production=increase in cystolic [ca2+] = contraction of smooth muscle

Question 24

What effect do local metabolites have on vasulature?

Answer 24

Cause vasodilation - ensure adequate perfusion of skeletal and coronary muscle .

*H+, k+, adenosine- metabolites all need to be removed before too much vasodilation occurs

Question 25

How do the baroreceptors work?

Answer 25

They are sensitive to stretch. Ion channels that are activated upon stretching cause firing of action potentials down the afferent pathways.

Question 26

What can the baroreceptors in the heart not do?

Answer 26

Maintain blood pressure over long periods of time. Baroreceptors can re-set to higher levels with persistent increases in blood pressure

Question 27

What are sympathomimetics? Give 2 examples.

Answer 27

Drugs that mimic the sympathetic NS

Eg alpha-adrenoreceptor agonists and beta-adrenoreceptors agonists

Question 28

What are the 3 main types of drugs that can act upon the autonomic nervous system?

Answer 28

Sympathomimetics (mimic-agonists)
Adrenoceptor antagonists (block)
Cholinergics (both- muscarinic)

Question 29

What are the cardiovascular uses of sympathomimetics? What is another use of these drugs?

Answer 29

• can give adrenaline to restore function in cardiac arrest (causes vasoconstriction in high conc because it works on the alpha 1 receptors in vessels)
• b1 agonist (selective)- may be given in cardiogenic shock (pump failure) ie dobutamine
• adrenaline administered for anaphylactic shock

Other uses;
-b2 agonist- ie salbutamol for treatment of asthma, causes dilation of airways

Question 30

What are the 2 classes of adrenoreceptors antagonists you can have to treat the heart? Give examples of both

Answer 30

Alpha adrenoreceptors antagonists;
1) alpha 1 antagonists eg prazosin
Possible anti-hypertensive agent but there are better things to use. (More likely to use an ACE inhibitor instead) Alpha 1 antagonists are used with resistant hypertension (when one is quite far down the line).
It inhibits NA action on vascular smooth muscle a1 receptors- stops vasodilation

Beta adrenoreceptors antagonists;
1)propranolol
Non selective b1/b2 antagonist, stops effect of NA therefore slows heart rate and -ve iontropic effect (b1), but will also cause bronchoconstriction…so DONT give to asthmatics!!
2) atenolol
Selective for b1 (cardio-selective)- less risk of bronchoconstriction

Question 31

What are the two types of cholinergic drugs you can use to act upon the heart? Give examples

Answer 31

Muscarinic agonists
[eg pilocarpine
-used in treatment of glaucoma- activates constrictor pupillae muscle]

Muscarinic antagonists
Eg atropine or tropicamide
-increase heart rate and bronchial dilation
(-used to dilate pupils for examination of the eye)