Lecture 14: The autonomic nervous system Flashcards
What is found in disease i.e CVD or renal failure and sympathetic nerve activity?
There is increased sympathetic drive to the muscles in these conditions
There is no increase in sensory sympathetic nerve activity.
What does the SNS tree indicate?
There can be a change in SNS drive to different organs at different levels.
What is the typical neurotransmitters of the SNS?
Ach
- Somatic peripheral nerves
- Autonomic ganglia
- Parasymp postganglionic fibres
Catecholamines
- Symp post ganglionic fibres
- Adrenal medulla
Where are nicotinic receptors found?
Skeletal muscle
Autonomic ganglia
Muscunaric (parasymp target tissue) (i.e muscarine)
What are nicotinic receptor antagonists?
Neuromuscular blockers: Drugs that are competitive antagonists at the Nm receptors cause neuromuscular blockade
i.e tubocurarine used as muscle relaxants during surgery
Ganglion blockers: Drugs that act as antagonists at Nn.
What are muscarinic antagonists?
Atropine:
- Reverses post MI transient increases in parasymp
- Increases SAN firing and conduction through AVN
What are the adernergic receptors? and what are their functions?
A1 = Blood vessels, Vasoconstriction A2 = CNS, Vasodialtion B1 = Heart atria and ventricles, HR and SV B2 = Vasculature, Vasodilation
What are agonists of adrenoreceptors?
a1 = Phenylephirine, oxymetazoline (vasoconstrictors) a2 = Clonidine, drops BP (less NA release, major central actions) b1 = Dobutamine, increased contractility (but causes dysrhythmias) b2 = salbutamol, bronchial dilator
What is the autonomic regulation of the cardiovascular system?
Parasympathetic system: Vagal control of HR
Sympathetic nervous system: HR, SV, CO and vascular tone
Describe the pacemaker cell depolarisation:
1) Pacemaker potential: The slow depolarisation is due to If current (Na driven mostly) (inwards funny current)
2) Depolarisation: At threshold, Ca channels open. Explosive Ca influx (ICaT) causes rapid depolarisation which is sustained by slow type Ca channels.
3) Repolarisation: Due to Ca channels inactivating and K channels opening.
- Unstable resting membrane potential
- Depolarisation due to relatively slow Ca current.
How is HR neurally controlled?
Via alteration of pacemaker potential
Describe the neural decrease of HR:
Vagal nerve (ACh) -> Decreases rate of spontaneous depolarisation and hyperpolarises the RMP (Inc K in, Dec. If)
Describe the neural increase of HR:
Symp (NA) -> Increases rate of spontaneous depolarisation (Inc. If and IcaT)
What happened to SNS activity during graded exercise post cardiac transplant?
- Resting HR is elevated
Response to exercise:
- Increase is delayed and blunted
- Dependant on level of circulating catecholamines not nerve activity as there are none.
Describe how B1 receptors increase SV;
NA acts via:
b1-> increase cAMP, thus phosphrylation by PKA =
- Increase Ca influx (L-type) during AP
- Increase Ca from SR (Due to increase SR Ca uptake via phospholambam
= Increase inotropy and thus inc SV
Describe how B1 receptors increase HR:
In SAN, cAMP augments opening of I(f) and ICaT channels. (As HR increases there is less time for Ca extrusion THUS also contributes to an increased force of contraction)
What are some beta blockers and why use them?
Atenolol, meoprolol etc
- Prevent arrhythmias
- Reduced workload in HF (lowers O2 needs)
- Reduced blood pressure
Also for:
- Performance anxiety
- Glaucoma
- Migranes
How do a1 receptors act on vasculature?
- Increased smooth muscle vascular tone
- a1-> G protein coupled receptors -> IP3 -> Smooth muscle contraction and vasoconstriction
What is an a1 antagonist and why use it?
i.e Prozosin
- Blocks G protein
- Inhibits IP3 production
= Relaxation of vascular SM
Crisis hypertensive intervention
Side effects of prozosin?
Orthostatic hypotension
Reflex tachycardia
Dizziness
Nasal congestion
How do B2 receptors work?
Act via cAMP to inhibit myosin light chain kinase = Vasodilation
Increase blood flow during exercise in response to circulating adrenalin
What are the key autonomic reflexes aimed at maintaining BP?
- Baroreflex- Rapid response to acute changes in pressure
- Chemreceptor reflexes - changes in O2, CO2, pH in blood
- CNS ischeamic response: Responds to high CO2 or low PH as a response to decreased brain blood flow to increase peripheral resistance.
What are the receptors in the baroreflex? and how do they respond?
Stretch receptors in the carotid sinus and aortic arch.
Increase afferent activity in response to an increase in stretch (arterial pressure). Sensory info conveyed in the glossopharyngeal and vagus nerve.
Use a flow diagram to describe the baroreflex:
Increased arterial pressure
- > Increased baroreceptor firing
- > Central processing in medullary CV control centers
- > Increases PSN activity, decreases SNS activity
- > Reduced HR and SV and vasodilation
What is the dive reflex?
Oxygen conserving response
- Apnea
- Peripheral vasocon and rise in BP (Inc in SNS activity)
- Bradycardia (Slowing HR due to reflex increase in efferent vagus nerve activity)
i.e both SNS and PNS activity rise.
What is the dive reflex in response to?
- Stimulation of afferent fibres of the 5th cranial nerve (Cold/Pressure on face)
- Central command (Apnea)
- Central/peripheral chemoreceptors (pH, pO2, pCO2)
Whats another example of reflexes of HR?
Respiratory sinus arrhythmia
- Lung stretch receptors
- Change in venous return (b.c pressure) -> bainbridge reflex
- Baroreceptor reflex (b/c reduced VR = Reduced CO)
All come together to produce altered HR
Note: Inspiration = decreased intrathoracic pressure increases venous return, this increases atrial stretch = bainbridge reflex and increased ejection = increased aorta pressure = baroreflex, all come together to increase HR
What is a condition that impact the ANS?
Diabetic neuropathy
Describe the distribution of parasymp and symp nerves in the heart:
PSN: SAN and AVN
SNS: SAN and AVN and Ventricles
