The autonomic Control Of The CVS Flashcards
The autonomic nervous system (ANS)
regulates many physiological functions
HR, BP, body temp - via homeostasis
Co-ordinates body’s response to stress and exercise
Largely outside voluntary control
Exerts control over
– smooth muscle (vascular and visceral)
– exocrine secretion
– rate and force of contraction in the heart
2 divisions of the ANS
Parasympathetic nervous system - long preganglionic neurone, short post ganglionic neurone - secretes ACTH at both synapses
Sympathetic nervous system - short preganglionic neurone, long postganglioic - secretes ACTH at pre and adrenaline/noradrenaline at post
This division is based on anatomical grounds
Some text books include a third division the enteric nervous system
– Network of neurones surrounding GI tract
– Is normally controlled via sympathetic and parasympathetic fibres
Functions of the autonomic NS
Regulates physiological functions – Examples: BP,
Where parasympathetic and sympathetic divisions both innervate a tissue they often have opposite effects
Sympathetic activity is increased under stress
Parasympathetic system is more dominant under basal conditions
Both work together to maintain balance
E.g. Airways of lungs - Receptor present is for SNS is ß2 - sympathetic stimulus relaxes and opens airways, PNS stimulus contracts the muscles and narrows airways - receptor for PNS is M3
Heart - SNS affect is increase rate and force an contractions via ß1 receptors, PNS affect is decrease rate of contraction via M2 receptors
SNS drive to different tissues is independent regulated - so SNS activity to the heart can be increase without increasing activity to the GI tract - on some occasions (fight or flight response) there can be a more coordinated response
Control of the CVS
The ANS controls
– heart rate
– force of contraction of heart
– peripheral resistance of blood vessels
What the ANS does not do
– The ANS does not initiate electrical activity in the heart
Denervated heart still beats, but at faster rate
At rest the heart is normally under vagal influence
PNS and SNS input to the heart
Parasympathetic input to the heart -
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
Sympathetic input to the heart - Postganglionic fibres from the sympathetic trunk
Innervate SA node, AV node and myocardium
– leading to the release of noradrenaline
Acts mainly on
The pacemaker of the heart
Cells in the sinoatrial node (SA node) steadily depolarise toward threshold
– this forms a slow depolarising pacemaker potential
– turning on a slow Na+ conductance (Iƒ– funny current)
– this in turn opens Ca2+ channels
AP firing in the SA node sets the rhythm of the heart - quickest to depolarise
Effect of ANS on pacemaker potentials:
Sympathetic effect on SA node is mediated by B1 adrenoreceptors
Gs G protein couple receptors present here
This increases AC stim, —> cAMP increase —> PKA increase
Which speeds up pacemaker potential
How does noradrenaline increase force of contraction? -
NA acting on
ANS effects on vasculature
most vessels receive sympathetic innervation
– exceptions
some specialised tissue eg erectile tissue have parasympathetic innervation
most arteries and veins have alpha-
Vasomotor tone allows for vasodilation to occur
Decreased SNS output leads to less adrenaline so less SNS stimulation therefore vasodilation
Increased SNS output leads to more adrenaline so more SNS stimulation therefore vasoconstriction thus increasing TPR
Some blood vessels have
Role of local metabolites
Active tissue produces more metabolites – 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
Overall control of CVS
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)
Alters activity of efferent nerves
Baroreceptor - Baroreceptors present in the carotid sins and the aortic arch are sensitive to stretch (stretch usually comes about in these regions due to increased pressure)
Once they sense this increase in stretch (increase BP) they send a stimulus via afferent pathways to the medulla which has negative regulation so it causes bradycardia and vasodilation therefore counteracting the increase in mean arterial pressure
Vice versa if baroreceptors sense a drop in stretch (BP)
The baroreceptor reflex is important for maintaining blood pressure over short term
It compensates for moment to moment changes in arterial BP
However Baroreceptors can re-set to higher levels with persistent increases in blood pressure (someone with hypertension) - body adapting to the changes seen
Clinical application - drugs acting on the ANS
Sympathomimetics
– alpha
Sympathomimetics
cardiovascular uses
– administration of adrenaline to restore function in cardiac arrest
–
Adrenoreceptor antagonists
adrenoreceptor antagonists
–
Cholinergics
Muscarinic agonists – e.g. pilocarpine – used in treatment of gluacoma - activates constrictor pupillae
muscle
Muscarinic antagonists – e.g. atropine or tropicamide
– increases heart rate, bronchial dilation – used to dilate pupils for
examination of the eye
