Autonomic Control Of CVS

Question 1

What does the autonomic nervous system control?

Answer 1

Physiological function:

• Heart rate, BP, Body temp.. ect (homeostasis)
• Coodinating the body’s responses to exercise and stress
• Largely outside voluntary control

Question 2

What tissues can the ANS exert control over?

Answer 2

Smooth muscle (vascular and visceral)
Exocrine secretion
Rate and force of contraction in the heart

Question 3

Differences between the sympathetic and parasympathetic control

Answer 3

Sympathetic: shorter preganglionic and longer postganglionic neurones

Parasympathetic: longer preganglionic neurones and very short postganglionic neurones.

Pre: release Ach which act on nicotinic receptors

Sympathetic post: Mostly noradrenaline (can be ACh or ATP..)

Parasympathetic post: ACh which act on Muscarinic ACh receptors.

Opposite effects. Sympathetic is increased under stress whereas parasympathic is more dominant under basal conditions.

Question 4

Examples of ANS control (Pupil, Airways, Heart, Sweat glands) under sympathetic and parasympathic control.

Answer 4

Pupil: S = dilation (contracts radial muscle) on A1 receptors. PS = Constriction (contracts sphincter muscle) M3 receptors

Airways: S= relax B2 PS= Contract M3

Heart: S= Increase rate and force of contraction B1 PS=Decreased rate M2

Sweat glands: S ONLY localised secretion A1 Generalised secretion M3 - ACh rather than noradrenaline.

Question 5

What does the autonomic nervous system control in the CVS?

Answer 5

It can control:

• Heart rate
• Force of contraction of heart
• Peripheral resistance of the blood vessels

Question 6

What does the ANS NOT do in the CVS?

Answer 6

It does NOT initiate electrical activity in the heart
-Denervated heart still beats but at a faster rate. This tells us the heart, at rest, is normally under vagal (parasympathetic) influence.

Question 7

Where does parasympathic innervation go to and originate from?

Answer 7

The preganglionic fibres come from the 10th cranial (VAGUS) nerve.
Synapse with postganglionic cells on epcardial surface or within the walls of the heart at the SA AND THE AV NODE!

Release ACh

Act on M2 receptors

• decrease heart rate (-ve chronotropic effect)
• Decrease AV node conduction velocity

Question 8

Sympathetic input to heart

Answer 8

Postganglionic fibres from the sympathetic trunk

Invervate the SA Node AV node and MYOCARDIUM.

Act on B1 adrenoreceptors.

• Increased heart are (+ chronotropic effect)
• AND increase force of contraction (+ inotropic effect)
• ALSO decrease speed of relaxation.

B2 and B3 adrenoreceptors are also present in toe heart but the main effect is mediated by B1 receptors.

Question 9

What are the pacemaker cells of the heart?

Answer 9

SA node as they depolarise the fastest.

They steadily depolarise towards the threshold.

• Slow depolarising pacemaker potential
• Turning on of a sow Na conductance (If- funny current)
• Opening of Ca channels

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

Question 10

What effect does ANS control have on pacemaker potentials

Answer 10

Sympathetic effects speed up depolarisation. Mediated by B1 receptors. G-protein coupled receptors (G alpha s) increase cAMP and speed up pacemaker potential.

Parasympathetic: Na channels open more slowly so decrease rate of depolarisation. Parasympathetic effect mediated by M2 receptors.
G-protein couples receptor (G alpha i)
Increase K+ conductance and decrease cAMP

Question 11

How does noradrenaline increase force of contraction?

Answer 11

NA acting on N1 receptors in myocardium caused n increase in cAMP - This activates Protein Kinase A

1. Phosphorylation of CA2+ channels increase Ca2+ entry during the plateau of AP
2. Increase uptake of Ca2+ in sarcoplasmic reticulum

• These lead to increased force of contraction.

Question 12

What are the effects of ANS on the vasculature

Answer 12

Most vesssels receive sympathetic inervation only. (Except specialised tissue - e.g. erectile tissue has parasympathetic innervation)

Most arteries and veins have A1-adrenoreceptors
-Coronary Arteries and skeletal muscle vasculature lots has B2-receptors.

Question 13

Vasomotor tone?

Answer 13

Vasomotor tone allows for vasodilation to occur.

This is by the effect of the A1 adrenoreceptors.

Vasoconstriction: Increase sympathetic output.
Vasodilation: Decrease output.

Question 14

Where are both A1 and B2 receptors present? What effect does this have?

Answer 14

Both these receptors present in skeletal muscle, myocardium and liver.

B2 has a higher affinity for adrenaline than A1.
At physiological conc. circulating adrenaline will preferably bind to B2 adrenoreceptors and cause vasodilation.

At higher concentration, it will also activate A1 receptors (pharmacological levels) therefore causing vasoconstriction.

Question 15

What happens when B2 adrenoreceptors are activated?

Answer 15

B2 adrenoreceptors cause vasodilation.
-Increases cAMP which activates Protein Kinase A. This opens K channels and therefore inhibits Myosin light chain Kinase. This causes relaxation of smooth muscle. VASODILATION

Question 16

What happens when B2 adrenoreceptors are activated?

Answer 16

It stimulates IP3 production
Increases in Ca conc. from stores and via Influx of extracellular Ca2+. This leads to contraction of smooth muscle and therefore VASOCONSTRICTION

Question 17

What is the role of local metabolites on vasculature?

Answer 17

Active tissue produce more metabolites - e.g. adenosine, K+, H+, increase PCO2

Local increases in metabolites have a strong vasodilator effects.

Metabolites all act to vasodilate.

Metabolites are more important for ensuring adequate perfusion of skeletal and coronary muscle than activation of B2-receptors.

Question 18

What are receptor afferents?

Answer 18

These help to maintain arterial BP when during things like standing up.

This is the baroreceptor reflex that relies on the stretch receptors

Question 19

What are baroreceptors?

Answer 19

Stretch receptors that are influenced by pressure.

Nerve ending in the carotid sinus and aortic arch are sensitive to stretch. This increased arterial pressure stretches these receptors.

Arterial BP increased then increased firing of baroreceptors.

Arterial BP decreased then decreased firing of baroreceptors.

This response is important for maintaining the blood pressure over the short term.

It compensates for moment to moment changes in arterial BP

Question 20

Problems with baroreceptors?

Answer 20

Baroreceptors can re-set at higher levels with persistence increases in blood pressure.

Question 21

Drugs?

Answer 21

Sympathomimemics mimic effects of sympathetic nervous system.
-a adrenoreceptor agonists or b-adrenoreceptor agonists

Adrenoceptor antagonists.

Cholinergics
-Muscarinic agonists and antagonists

Question 22

What are some uses of Sympathomimetics?

Answer 22

CV uses:
-Administration of adrenaline to restore function in cardiac arrest.
B2 agonist - Dobutamine - may be given in cardiogenic shock (pump failure)
Adrenaaline administered for anaphylactic shock.

Other:
Salbutamol - B2 agonist for asthma.

Question 23

Uses of Adrenoreceptor antagonists?

Answer 23

A receptor antagonists:

• A1 antagonists e.g. prazosin
• anti-hypertensive agent - inhibit NA action on vascular smooth muscle A1 receptor - vasodilation.

B-adrenoreceptor antagonists

• Propranolol - non-selective B1/B2 antagonist. SLows heart rate and reduces the force of contraction (B1) but also acts on bronchial smooth muscle (B2) - Bronchoconstriction.
• Atenolol - Selective B1 (cardio-selective) - less risk of bronchoconstriction.

Question 24

Uses of choliergics?

Answer 24

Muscarinics agonists w.g. Pilocarpine is used in the treatment of glaucoma as it activates the constrictor pupilae muscles.

Muscarinic antagonists e.g. atropine or tropicamide which increases heart rate, bronchial dilation. This can be used to dilate pupils for examination of the eye.