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RUSH - ADVANCED PHARMACOLOGY - NSG 531 - EXAM 3
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RUSH - ADVANCED PHARMACOLOGY - NSG 531 - EXAM 3
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RUSH - ADVANCED PHARMACOLOGY - NSG 531 -EXAM 3
What is the difference between cardiac myocyte action potential and that of the CNS or
ANS? - Answers-nerve cell action potential is very short
Cardiac action potential is much longer
They are longer to have adequate filling time in order to get a good contraction for a
reasonable bolus of blood
The only way this can happen is if the action potential is longer
This will also mean that the refractory period will be longer
What are the 5 phases of the non-pacemaker action potential? - Answers-0 -
depolarization
1 - partial repolarization
2 - plateau
3 - repolarization
4 - resting membrane potential
What happens during phase 0 of the non-pacemaker action potential - Answers-
depolarization
Voltage gated sodium channels are opening up until we get past threshold
What happens during phase 1 of the non-pacemaker action potential - Answers-partial
repolarization
When does contraction take place? - Answers-begins towards the end of repolarization
and ends at some point during repolarization
Refractory period - Answers-during phase 0, 1, 2, and part of phase 3 the cell is
refractory to the initiation of new action potentials
Many antiarrhythmic drugs increase the Refractory period which reduces myocyte
excitability
What are the benefits of the refractory period - Answers-limits frequency of cardiac
contractions
Allows for adequate filling time
Prevents sustained contractions
How are pacemaker cells different from non-pacemaker cell - Answers-no resting
membrane potential - no point where it is flat
There are very few sodium channels in pacemaker - sodium channels are not driving
depolarization - calcium is
Only 3 phases
Comprised of cells within the SA node
,Generate regular, spontaneous action potentials
What are the phases of pacemaker action potential - Answers-0 - rapid depolarization
3 - repolarization
4 - slow depolarization
What happens during phase 0 of the pacemaker action potential - Answers-Rapid
depolarization
Something is coming to open voltage gated calcium channels (L-type) calcium comes
rushing in
What happens during phase 3 of the pacemaker action potential - Answers-
repolarization
Potassium channels now open up, potassium rushes out, repolarizes
What happens during phase 4 of the pacemaker action potential - Answers-slow
depolarization
With potassium rushing out we are all the way down at -60
Funny sodium channels open up until voltage reaches -50
T-type (transient) calcium channels open up until voltage reaches -40
L-type calcium channels then open back up
What happens during phase 2 of the non-pacemaker action potential - Answers-plateau
Calcium channels open (L-type because they are long)
Potassium is still open
Potassium out and calcium in - they are opposing each other in voltage giving the
plateau
This is when the ventricles are filling
What happens during phase 3 of the non-pacemaker action potential - Answers-
repolarization
Calcium channels are closed
Potassium channels are the only thing open taking their positive charge with them
making the interior more negative
What happens during phase 4 of the non-pacemaker action potential - Answers-resting
membrane potential where we are in between action potentials there is no net change in
ovltage inside the cell
Describe how non-pacemaker aps can mimic pacemkaer aps - Answers-Hypoxia and
ischemia
When the resting membrane potential is not getting enough oxygen it is going to
become more positive because you need oxygen to produce ATP. If we are deficient in
ATP then the NA K atpase pump wont be functioning
, If someone is hypoxic in a focal area - say they have a resting membrane potential at -
45 - the fast sodium channels won't open - they start using calcium to open - so they
would convert into action potentials that use calcium (hence how they mimic pacemaker
aps)
Excitation-contraction coupling - Answers-sequence of events from motor neuron
signaling to a skeletal muscle fiber to contraction of the fiber's sarcomeres
Conversion of depolarizing currents into contractile force
L-type calcium channels open up in phase 2 in nonpacemaker - calcium comes flooding
into myocytes, so we now have calcium in the cell and a sarcoplasmic recticulum (a
resovior for calcium)
Receptors called RYR (ligand gated calcium channels)
Calcium then comes out - coming int the cell from the calcium channels and the
sarcoplasmic recticulum
Describe how calcium binds to cause contraction - Answers-when there is an influx of
calcium in the cell there is a myosin head separated by troponin. Little binding sites for
the myosin exist on the aktin but it can't get to it because of the troponin. Calcium
therefore binds to the tropinin causing a confirmational change in troponin so it will
move and take the tropomyosin with it. The myosin can then bind to the aktin molecules
when it binds it activates ATP
The ATP will be used to generate the sliding of the aktin and the myosin filaments
against each other shortening the muscle cell causing contraction
Describe how adrenergic stimulation increases the force of contraction through inotropic
effects - Answers-NE and epi bind to adenylyl cyclase coupled g proteins (beta 1)
Leads to phosphorylation of Ca channels and opens them
Increases inward movement of Ca
There is also increased release of Ca from the SR
Increases actin/myosin interaction
Increases force of contraction
Describe how adrenergic stimulation increases the force of contraction through
chronotropic effects - Answers-NE and epi bind to adenylyl cyclase coupled g proteins
(beta 1)
Results in phosphorylation of Ca2 channels and opens them
Increases inward movement of Ca2
Shortens phase 0 by increasing the opening of L-type calcium in pacemaker
Heightened sympathetic state
Shortens effective refractory period
Increases rate of contraction
How do catecholamines effect the nak atpase Pump - Answers-epi to beta 1 - g coupled
protein receptor
Increase in camp
Activate protein kinase
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