CVS ANS and Action Potentials Flashcards
State the differences between the SNS and PNS
SNS:
Thoraco-lumbar outflow (all 12 T, first 2 L)
Short pre, long post
Preganglionic are cholinergic (nicotinic)
Postganglionic are noradrenic (except perspiration + ejaculation pathways which are cholinergic)
PNS:
Cranio-sacral outflow
Long pre, short post
Preganglionic are cholinergic (nicotinic)
Postganglionic are cholinergic (muscarinic)
State the distribution of different types of adrenoreceptor around the body
Heart: SNS B1, PNS M2
Airways: SNS B2, PNS M3
Pupils: SNS a1, PNS M3
Sweat glands: SNS localised secretion is a1, general secretion is M3 (no PNS innervation)
What is the action of the SNS on blood vessels in different organs?
The SNS innervates smooth muscle in blood vessel walls
It causes vasoconstriction via a1-adrenoreceptors
There is constant SNS activity - vasomotor tone.
Vasomotor tone in skin is high so arterioles and pre-capillary sphincters are generally closed
Vasomotor tone in skeletal muscle is high at rest but antagonised by vasodilators during exercise
In the gut vasomotor tone is high until meal consumption
What is the action of the SNS and PNS on the heart?
Both innervate SA and AV nodes so affect HR
Centres in the medulla oblongata receive information from baroreceptors in the aortic arch and carotid sinuses
If all autonomic input to the heart is blocked heart rate would be ~100bpm, therefore PNS dominates SNS at rest
Initial increase in heart rate is due to reduction in parasympathetic outflow
Sympathetic nerve fibres innervate ventricular cadiac myocytes and increase force of contraction
Sympathetic - NA - B1receptors
Parasympathetic - ACh - M2receptors
How is the resting membrane potential generated?
Cell membrane of myocardial cells is mostly permeable to K+ ions so the cardiac resting potential is ~ -90mV
How do changes in the membrane permeability result in changes to the membrane potential in ventricular cells?
Diastole (4): membrane potential close to Ek
Initial depolarisation is due to spread of electrical activity from pacemaker cells. Once threshold reached, voltage gated Na+ channels open causing rapid depolarisation (0)
A breif repolarisation is caused by outflow of K+ back to a membrane potential of 0mV (1)
There is a plateau as sodium channels deactivate but depolarisation opens Ca2+ channels that keep the cell depolarised (2)
Influx of calcium causes CICR (calcium induced calcium release) causing contraction
Ca2+ channels close and efflux of K+ return potential to resting (3)
How do changes in the membrane permeability result in changes to the membrane potential in pacemaker cells?
The lowest voltage of pacemaker cells is ~ -60mV which keeps the fast Na+ channels inactivated
The spontaneous gradual depolarisation (pacemaker/funny current) is due to opening of slow Na+ channels that open during cell repolarisation. (HCN channels - hyperpolarisation-activated Cyclic Nucleotide gated channels)
Once threshold is reached Ca2+ channels open giving slow depolarisation (fast Na+ channels inactive)
Ca2+ channels close and the cell repolarises due to efflux of K+
How do changes in the membrane potential result in increases and decreases of heart rate?
Increasing HR:
Action of the SNS on the SAN
NA (B1 receptor) increases HR by making the pacemaker potential steeper so reaches threshold quicker
Decreasing HR:
Action of the PNS on the SAN
ACh (M2 receptor) slows HR by making the pacemaker potential shallower
Increases K+ conductance
How does NA increase the force of contraction in the heart?
NA acts on B1 receptors causing an increase in cAMP which activates PKA:
- Phosphorylates Ca2+ channels which increase Ca2+ entry during AP plateau
- Increase uptake of Ca2+ in SR to reduce length of contraction
- Increased sensitivity to Ca2+
Give a broad overview of the types of drugs acting on the ANS
Sympathomimetics (mimic SNS) e.g. a & B adrenoreceptor agonists
Adrenoreceptor antagonists
Cholinergics e.g. muscarinic agonists and antagonists
What are some clinical uses of sympathomimetics?
Cardiovascular uses: adrenaline to restore function in cardiac arrest act on a1 and B1
DOBUTAMINE (B1 agonist) given in cardiogenic shock
B2 aganost Salbutamol used for asthma, relaxes brachial smooth muscle
What are some clinical uses of adrenoreceptor antagonists?
a antagonists:
PRAZOSIN is anti-hypertensive as it inhibits NA action on smooth muscle causing vasodilation
B antagonists:
Propanolol (non selective) slows HR (B1) but also constricts bronchiole smooth muscle (B2)
Atenolol (selective to B1 so cardio-selective) less is of bronchioconstriction
What are some clinical uses of cholinergics?
Muscarinic agonists:
e.g. Pilocarpine
Used to treat glaucoma by activating constrictor papillae muscle
Muscarinic antagonists:
e.g. atropine or tropicamide
Used to dilate pupils for eye examinations
