Autonomic Control Of The CVS

Question 1

What receptor is stimulated in the pupil of the eye by the sympathetic nervous system ?

Answer 1

A1- which causes dilation of the pupils due to contraction of the radial muscle.

Question 2

Which receptor is stimulated in the pupil of the eye under parasympathetic influence ?

Answer 2

M3- this causes contraction of the pupil of the eye due to contraction of the sphincter muscle

Question 3

What receptor is stimulated in the airways under sympathetic influence ?

Answer 3

B2- which causes the airways to relax.

Question 4

What receptors are activated in the airways of the lungs under parasympathetic influence ?

Answer 4

M3- which causes the smooth muscle to contraction.

Question 5

What receptors are activated in the heart under sympathetic influence ?

Answer 5

B1 which increases the rate and FORCE of contraction.

Question 6

What receptors are activated in the heart during parasympathetic influence ?

Answer 6

M2- which causes a decrease in the heart rate,

Question 7

What receptors are activated in the sweat glands under sympathetic influence - for example when we are nervous ?

Answer 7

A1- this causes sweaty palms / armpits when nervous.

M3 receptors are activated for generalised secretions.

Question 8

Is the sweat gland under parasympathetic control ?

Answer 8

NO

Question 9

What does the autonomic nervous system control in terms of the CVS?

Answer 9

1) heart rate
2) force of contraction
3) peripheral resistance of blood vessels

Question 10

Does the autonomic nervous system initiate electrical activity in the heart ?

Answer 10

No

Question 11

Would the heart rate increase or decrease , when the heart is denervated ?

Answer 11

Increase , this is because usually the is under the influence of the vagus nerve ( parasympathetic influence ) which allows a slower heart rate.

Question 12

What is the tenth ( X) cranial nerve called ?

Answer 12

Vagus nerve

Question 13

Outline the parasympathetic input to the heart

Answer 13

• preganglionic fibres of the vagus nerve synapse with the postganglionic cells on the epicardial surface or within the walls of the heart at the SA/AV node.
• the postganglionic cells release ACH.
• the ACH acts on the M2 receptors in the heart which works to decrease heart rate ( negative chronotropic effect ) and decrease AV node conduction velocity.

Question 14

Outline features of the sympathetic input to the heart

Answer 14

• post ganglionic fibres from the sympathetic drink inner fates the SA node , AV node and mycocardium.
• releases noradrenaline and acts mainly on B1 adrenoreceptors which increases heart rate ( positive chrontropic effect) , and increases force of contraction ( +ve inotropic effect)

Question 15

Are there any other beta receptors in the heart - other than B1?

Answer 15

B2 and B3 adrenoreceptors are also present in the heart but the main effect is mediated by b1 adrenoreceptors.

Question 16

How does sympathetic/parasympathetic stimulation of th heart affect action potentials in the SA node ?

Answer 16

• Sympathetic activity increases the steepness of the depolarising slope ( funny current ).
• this is because sympathetic effect mediated by B1 adrenoreceptors which are G protein coupled receptors which increases cAMP. Which speeds up pacemaker potential.

WHEREAS with the parasympathetic activity , it would decrease the steepness of the slope. The effect is mediated by M2 receptors. Which are G protein coupled receptors which increase K+ conductance ( so it is harder to get to threshold ) and decrease CAMP.

Question 17

How does noradrenaline increase the force of contraction of the heart ?

Answer 17

1) noradrenaline acts on B1 receptors in the myocardium which causes an increase in cAMP. cAMP goes off to activate protein kinase A.
2) protein kinase A in responsible for the phosphorylation of VOCC ( voltage operated calcium channels). Which causes an influx of Ca2+ because this channel is remained open for longer. This influx causes calcium inducer receptors ( eg ryanodine ) on the surface of the SR to activate which causes an increase release of Ca2+.
3) this leads to an increased force of contraction.

Question 18

Do vessels mainly receive sympathetic or parasympathetic innervation?

Answer 18

Sympathetic innervation except some specialised tissue for example erectile tissue which have parasympathetic innervation.

Question 19

Most arteries and veins have which type of receptors?

Answer 19

A1- adrenoreceptors but coronary and skeletal muscle vasculature also have B2 receptors.

Question 20

Under normal psychological conditions where there needs to be a normal level of vascular tone , what hormone is released ?

Answer 20

Noradrenaline

Question 21

When there is a decreased sympathetic output, what occurs to the vessels ?

Answer 21

• there is a decreased release of noradrenaline which results in vasodilation.

Question 22

When there is an increased sympathetic output , what occurs to the vessels ?

Answer 22

They vasodilation because there is an increased release of noradrenaline.

xxxx

Question 23

What type of blood vessels also contain b2- adrenoreceptors as well as A1?

Answer 23

Skeletal muscles

Myocardium

Liver

Question 24

At physiological concentration circulating adrenaline will preferentially bind to which type of receptor in blood vessels ?

Answer 24

B2 adrenoreceptors which would initiate vasodilation.

This is because circulating adrenaline has a higher affinity for b2 adrenoreceptors than a1 receptors.

Question 25

At higher concentrations of adrenaline * ( eg during fight or flight or exercising) - what receptors would adrenaline bind to ?

Answer 25

A1 receptors which would cause vasoconstriction.

Question 26

What are the effects of activating B2- adrenoreceptors in the smooth muscle of vessels ?

Answer 26

B2 receptors are G(s) protein coupled receptors. 2) This would increase production of cAMP from ATP. This would result in the activation of protein kinase A. 3) Protein kinase A opens potassium channels and inhibits MLCK ( myosin light chain kinase) which causes relaxation of the vascular smooth muscle as this prevents the interaction between actin and myosin. Thus vasodilation.

Question 27

What are the effects of activating A1 adrenoreceptors in the vascular smooth muscle of vessels ?

Answer 27

1) A1 receptors are G(q) protein coupled receptors. 2) once activated , this activated phospholipase C enzymes which hydrolyses PIP2 into IP3 and DAG. 3) IP3 is responsible for the increase of Ca2+ from stores . Which results in contraction of smooth muscle THIS RESULTS IN VASOCONSTRICTION.

Question 28

What sort of metabolites do active tissue produce ?

Answer 28

Adenosine k+ H+ Increase in PCO2

Question 29

What is the importance of local metabolites increasing ?

Answer 29

They have a strong vasodilator effect - they are more important for ensuring adequate perfusion of skeletal and coronary muscles than activation of B2-receptors .

Question 30

Where are baroreceptors found ?

Answer 30

1) carotid sinus | 2) aortic arch

Question 31

What do baroreceptors detect ?

Answer 31

Changes in arterial pressure because they are sensitive to stretch.

Question 32

Outline the baroreceptors reflex when arterial blood pressure is high ?

Answer 32

1. Baroreceptors in the carotid sinus or aortic arch would be stretched. 2. A signal would then be sent along an afferent pathway to the medulla oblongata ( at the base of the brain). Which acts as a co ordinating centre. 3. This would then be signalled along the efferent pathways ( eg the vagus nerve) to effectors such as the heart and vessels. 4. This would cause bradychardia and vasodilation to counteract the increased mean arterial pressure.

Question 33

Is the barorecetor reflex important in maintaining blood pressure over short term or long term ?

Answer 33

Short term

Question 34

Give an example of a muscarinic antagonist ?

Answer 34

Atropine or tropicamide which increases heart rate , bronchial dilation? - used to dilate pupils for examinTions in the eye.

Question 35

Give examples of muscarinic agonists ?

Answer 35

Pilocarpine which is used in treatment for gluacome which activates constrictor pupillae muscles.

Question 36

Give examples of a-adrenoreceptors antagonists ?

Answer 36

A1-antagonist eg prazosin. Which is used as a hypertensive treatment. As it inhibits noradrenaline action on vascular smooth muscle allowing vasodilation.

Question 37

Give examples of B-adrenoreceptors antagonists ?

Answer 37

Propranolol which is a non selective B1/B2 antagonist. - this slows the heart rate and reduced force of contraction (B1) but also acts on bronchial smooth muscle ( bronchoconstriction). - ATENOLOL. Which is a selective b1 anatagonist which lessens the risk of bronchoconstriction

Question 38

What are sympathomimetics?

Answer 38

Drugs that mimic the effects of th sympathetic nervous system. For example a-adrenoreceptors and b-adrenoreceptors agonists

Question 39

Giv examples of sympathomimetics

Answer 39

Administration of adrenaline to restore function in cardiac arrest. - B1 agonist - dobutamine may be given in cardiogenic shock - Adrenaline is administered for anaphylactic shock ( a1- smooth muscle contraction which improves circulation of blood flow ) B1- heart muscle contraction and smooth muscle relaxation (B2).