The ANS and the CVS Flashcards Preview

Cardiovascular System > The ANS and the CVS > Flashcards

Flashcards in The ANS and the CVS Deck (24):

Describe the breakdown of the ANS and where the two type of ganglionic neurons for each NS are found.

ANS has two parts – SNS and PNS. Both have preganglionic neurons in the CNS and postganglionic neurones in the Peripheral nervous system.


Where is the sympathetic nervous system derived from and where does its post ganglionic neurons synapse?

The sympathetic nervous system is thoracolumbar derived and synapses with its postganglionic neurones in the para or prevertebral sympathetic chain.


Where is the parasympathetic nervous system derived from and where does its postganglionic neurons synapse?

The parasympathetic nervous system comes from the craniosacral segments and synapse with postganglionic neurones very close to their target organ, making PNS postganglionic neurones very short.


What neurotransmitter do all preganglionic neurons release and what's special about the receptor for this transmitter?

All preganglionic neurones release acetylcholine acting on nicotinic acetylcholine receptors which have an intrinsic ion channel allowing K+ out and Na+ in.


What do SNS/PNS postganglionic neurons release and what are the exceptions?

SNS postganglionic neurones are most commonly noradrenergic (exception for sweat glands and hair follicles – ACh muscarinic), whilst PNS postganglionic are usually cholinergic (muscarinic).


What is special about the SNS in the adrenal medulla?

In Adrenal medulla chromaffin cells act like specialised post ganglionic neurones and when stimulates by ACh they release adrenaline into the blood stream.


What are the 4 types of adrenergic receptors, their corresponding G proteins and the main enzyme they effect.

Noradrenaline and adrenaline act on adrenoreceptors, there are 4 types:
Alpha 1 (Gq - PKC)
Alpha 2 (Gi - adenylyl cyclase then PKA)
Beta 1 (Gs - adenylyl cyclase then PKA)
Beta 2 (Gs - adenylyl cyclase then PKA)


What are Co transmitters and give some examples?

Other transmitters than are released with NA such as ATP, NO and serotonin.


How does the SNS and PNS interact with each other?

Usually SNS and PNS have opposite effects where they both innervate, in times of stress SNS overrides PNS and under normal conditions PNS is dominant.


Describe the PNS innervation of the heart and it's effects.

CVS system is innervated by the vagus nerve (this is PNS), it synapses with postganglionic cells on epicardial surface, within walls of the heart, at the SA node and the AV node. They release ACh which acts on M2 receptors causing decrease in heart rate (negative chronotropic) and decrease AV node conduction rate.


What are the 3 types of Cholinergic receptors, their corresponding G proteins and the main enzyme they effect.

M1 - Gq - PKC
M2 - Gi - PKA
M3 - Gq - PKC


Describe the SNS innervation of the heart and it's effects.

Sympathetic input comes from the sympathetic trunk which innervates the SA and AV nodes and the myocardium releasing Noradrenaline. This acts on B1 receptors causing increase heart rate and increase force of contraction.


How does the stimulation of B1 and M2 receptors change the heart?

B1 adrenoreceptors are linked to G alpha s, stimulating the release of cAMP whilst M2 are G alpha I and inhibit the release of cAMP and increase K+ conductance. cAMP changes the slope of the pacemaker potential as the Sodium channels are sensitive to cAMP. B1 also increases force of contraction as cAMP activates PKA which phosphorylates Ca++ channels and increases Ca++ entry during the plateau, it also increases Ca++ storage and the sensitivity of the contractile machinery to Ca++.


Which tissues don't receive innervation from the SNS?

Erectile Tissue which has parasympathetic innervation.


What adrenoreceptors does most vasculature have?

Most arteries and veins have A1 adrenoreceptors but the coronary and skeletal muscle vasculature also have B2.


What is vasomotor tone?

Normal levels of output by the sympathetic nerves to blood vessels with A1 receptors gives us a vasomotor tone.


What happens when the levels of sympathetic innervation to vasculature change

Increasing sympathetic output increases muscle contraction and leads to vasoconstriction and the opposite to cause vasodilation.


Describe the mechanism of action of the activation of B2 receptors in vasculature.

Activating B2 receptors increase cAMP which stimulates PKA which in turn opens K+ channels and inhibits MLCK causing the relaxation of smooth muscle.


Explain the effect of adrenaline on vasculature.

Those vessels also containing B2 receptors are stimulated by circulating adrenaline (really high will also act on A1 receptors). This causes the muscles to relax leading to vasodilation. Action on A1 receptors by adrenaline will still cause vasoconstriction (hence how an epi pen works). This is not the main way vasodilation/constriction works.


Describe the mechanism of action of the activation of A1 receptors in vasculature.

Activating A1 receptors stimulates IP3 production which increases Ca2+ stores that come in causing cellular contraction.


What are the most important vasodilators in maintaining perfusion to tissues.

Local metabolites like adenosine, K+, H+ and CO2 all have a strong vasodilator effects and are more important in ensuring adequate perfusion of skeletal and coronary muscles than the A1 and B2 receptors.


Where in the brain is the sympathetic outflow to different areas of vasculature controlled.

Sympathetic outflow to different organs is controlled in the brain stem by the vasomotor centres in the medulla oblongata.


Describe the difference between the brain, skin and muscle in terms of their innervation by the ANS.

Vessels in the brain are virtually unaffected by ANS whilst the skin and skeletal muscles vary a lot and are used to control total peripheral resistance.


Where in the body are the main baroreceptors found and how do they work?

The receptors for blood pressure are found in the aortic arch and carotid sinuses, low blood pressures will cause fewer action potentials to reach the cardiac centres of the medulla whilst high will cause the opposite.