Session 5: Autonomic Control of the CVS

Question 1

Give examples of what the ANS is regulating.

Answer 1

Homeostasis such as heart rate, BP, temperature.

Responds accordingly to exercise and stress.

Question 2

What types of tissues are controlled by the ANS?

Answer 2

Smooth muscle
Exocrine secretion (glands)
Rate and force of the heart (cardiomyocytes)

Question 3

What is the sympathetic/parasympathetic effect on the pupil of the eye? Which receptors are activated?

Answer 3

Symp - Dilation (a1)

Para - Contraction (M3)

Question 4

What is the sympathetic/parasympathetic effect on the airways of lungs? Which receptors are activated?

Answer 4

Symp - Relax (b2)

Para - Constriction (M3)

Question 5

What is the sympathetic/parasympathetic effect on the heart? Which receptors are activated?

Answer 5

Symp - Increased rate (chronotropic) and force of contraction (inotropic) (b1)
Para - Decreased rate (M2)

Question 6

What is the sympathetic/parasympathetic effect on sweat glands? Which receptors are activated?

Answer 6

Symp - Localised secretion (a1)
Generalised secretion (M3)
Para - no effect

Question 7

The sympathetic nervous system to different tissue is independently regulated. What does this mean?

Answer 7

That the sympathetic activity in one tissue can be increased without affecting other tissue. However coordination occurs during fight to flight for example.

Question 8

What happens to the heart if you denervate it?

Answer 8

The ANS doesn’t initiate electrical activity in the heart. This means that a denervated heart still beats, however at a faster rate.

Question 9

Why would a denervated heart beat at a faster rate?

Answer 9

Because at rest the heart is normally under vagal influence meaning that the parasympathetic dominates.

Question 10

Explain the parasympathetic input to the heart.

Answer 10

The preganglionic fibres are from the 10th (X) cranial nerve called the Vagus (X) nerve.
The synapses of the postganglionic cells are on the epicardial surface within the walls of the heart at SA and AV node. Postganglionic AND preganglionic cells both release ACh.
ACh acts on M2 receptors which decreases heart rate and decrease AV node conduction velocity. The decreased heart rate is a negative chronotropic effect.

Question 11

Explain the sympathetic input to the heart.

Answer 11

Postganglionic fibres come from the sympathetic trunk. The fibres innervate the SA node, the AV node and the myocardium. The postganglionic fibres release noradrenaline.
The NA acts mainly on B1 to increase heart rate (positive chronotropic effect) and increases force of contraction (positive inotropic effect).
B2 and B3 adrenoreceptors are also present in the heart but mainly B1 are activated.

Question 12

Explain the pacemaker of the heart.

Answer 12

Cells in the sinoatrial node steadily depolarise toward the threshold. There is a slow depolarisation by turning on of a slow Na+ conductance called funny current. It means that Na+ slowly opens at in response to hyperpolarisation (-60 mV). Eventually Ca2+ channels will open.

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

Question 13

How does the ANS affect the pacemaker potentials?

Answer 13

Sympathetic - increases the slope of depolarisation meaning it will speed it up. Higher AP frequency.
Parasympathetic - decreases the slope meaning it will slow down. Lower AP frequency.

Question 14

How does NA increase force of contraction?

Answer 14

NA acts on beta1 receptors on myocardium causing an increase in cAMP that will activate PKA.
Phosphorylation of Ca2+ channels increases Ca2+ entry during the plateau of the AP.
Also there is an increased uptake of Ca2+ in SR.

Question 15

How does the ANS affect vasculature?

Answer 15

Most vessels receive only sympathetic innervation, there are some exceptions like erectile tissue but mainly vasculature is solely sympathetic.

Question 16

What kind of receptors do most arteries and veins have?

Answer 16

Alpha1-adrenoceptors

Question 17

Are there any exceptions?

Answer 17

Coronary, skeletal, myocardium and liver vasculature also have beta2 receptors.

Question 18

What is vasomotor tone?

Answer 18

The ‘normal’ dilation/constriction of vasculature.

Question 19

How is vasomotor ton increased or decreased?

Answer 19

Usually solely by either increase or decrease in sympathetic output. A decrease causes vasodilation and an increase causes vasoconstriction. This is by binding to alpha1 receptors.

Question 20

What does activating b2 adrenoceptors do? Explain the mechanism.

Answer 20

It causes vasodilation.

Increased cAMP -> PKA -> opens K+ channels and inhibition of MLCK -> relaxation of smooth muscle.

Question 21

What does activating alpha-1 adrenoceptors do? Explain the mechanism.

Answer 21

It causes vasoconstriction.
Stimulation of IP3 production which will cause influx of Ca2+ extracellularly and intracellular from SR leading to contraction of smooth muscle.

Question 22

What are the roles of local metabolites?

Answer 22

The active tissue produces more metabolites like adenosine, K+, H+ and PCO2.
Those local metabolites have a strong vasodilator effect.
Metabolites are more important for ensuring adequate perfusion of skeletal and coronary muscle than activation of beta2-receptors.

Question 23

What are baroreceptors?

Answer 23

They are nerve endings in the carotid sinus, and aortic arch. They are sensory neurons which are afferent going to the medulla oblongata. An increase in arterial pressure causes stretching in the carotid sinus and aortic arch. This stretch activates the receptors sending signal to the medulla oblongata. Medulla oblongata sends signals to heart and vasculature to cause bradycardia and vasodilation to counteract the mean arterial pressure.

Question 24

Why are not baroreceptors effective long term?

Answer 24

Because they can re-set/recalibrate to higher levels with a persistent increase in blood pressure.

Question 25

Give examples of drugs acting on the ANS.

Answer 25

Sympathomimetics like alpha and beta adrenoceptor agonists.

Adrenoceptor antagonists

Cholinergics - muscarinic agonists and antagonists

Question 26

Outline sympathomimetics uses.

Answer 26

Cardiovascular uses such as administration of adrenaline to restore function in cardiac arrest or administered for anaphylactic shock.
B1 agonist such as dobutamine can be given in cardio genie shock where there is pump failure.

B2 agonist - salbutamol for treatment of asthma

Question 27

Outline uses of adrenoreceptor antagonists.

Answer 27

alpha adrenoceptor antagonists such as Prazosin and anti-hypertensive agent. Inhibits NA action on vascular smooth muscle alpha receptors causing vasodilation.

Beta-adrenoceptor antagonists like propranolol that is a non-selective B1/B2 antagonist which slows heart rate and reduces force of contraction (B1) but also acts on bronchial smooth muscle (B2) causing bronchoconstriction.

Also atenolol which is a selective beta1 cardio-selective which poses less of a risk of bronchoconstriciton.

Question 28

Outline uses of cholinergics.

Answer 28

Muscarinic agonists like pilocarpine that is used in treatment of glaucoma that activates constrictor pupillae muscle.

Muscarinic antagonists - like atropine or tropicamide that increases heart rate and bronchial dilation. Also used to dilate pupils for examination of the eye.