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