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BIOC33H3 Lecture Notes - Reuptake, Cytosol, Endoplasmic Reticulum

Biological Sciences
Course Code
Stephen Reid

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BIOC34/BIOC33 Lec 5. Jan. 20/2014
oJust need to submit what is requested in instructions
Cardiac output
oAmount of blood pumped per unit time
oCO = SV x HR
Autonomic regulation of heart rate
oHave both types of parasympathetic innervation through vagus nerve
oFrom brainstem, have a branch of the vagus nerve that innervates pacemaker (SA
node) as well as a branch innervating the AV node connecting the electrical axis
of atria to the ventricle
oHave sympathetic nerve which also innervates the SA and AV nodes but it
innervates ventricular myocardium as well
oVentricular muscle has 2 purposes:
Increase force of contractility
Helps to speed up the relaxation of the heart when it transitions from
systole to diastole
Important because it allows heart to spend more time in diastole -
can fill with more blood
Autonomic regulation of heart rate
oParasympathetic (Vagus) : Have our cardiac branch of the vagus nerve that
presynaptically releases acetylcholine onto ganglia where it binds to nicotinic
receptors. Post-ganglionic cell also releases acetylcholine onto the heart.
Acetylcholine interacts with muscarinic acetylcholine receptor (on the heart)
In this case, see it slows down the rate of depolarization of pacemaker
cells and slows rate of conduction (waves of conduction from AV node)
oSympathetic system does the opposite - have ACh released from preganglionic
fibres onto ganglia
From post-ganglionic fibre have NE released as a neurotransmitter

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NE speeds up pacemaker potential as well as speeds up conductivity from
the AV node
oAdrenal gland - also under control of sympathetic nervous system. Pre-ganglionic
NT = ACh, reacts with nicotinic receptors on adrenal cells and release NE and
epinephrine into the blood. These hormones have similar effects or opposite
effects on the blood vessels. It depends on which organ is being talked about and
at what concentration
Sympathetic regulation of heart rate
oSpeeds up depolarization of pacemaker cells and speeds up conductivity through
AV node
oDoes this by enhancing influx of Na and Ca into the pacemaker cells or AV node
cells, allowing for more rapid depolarization
oWhen talking about NT from sympathetic nerve, it would be NE. if talking about
hormone from adrenal gland, would be both E and NE. They interact with beta-
adrenergic receptor on the cell membrane activating a stimulatory G protein,
which then activates AC, which catalyzes conversion of ATP into cAMP and
cAMP leads to phosphorylation of protein kinase.
oThis then activates our funny channels which allow Na in and some K out during
the first half of the pacemaker potential. More channels opening = more Na
influx. Also enhance opening of T-type Ca2+ channels, which are responsible for
the depolarization of the second half of the pacemaker potential.
oIn that slow pacemaker potential, have funny channels opening in the first half, T-
type channels opening in the second half, and the AP carried by Ca current
through L-type Ca channels.?? By having enhanced Na and Ca currents, have an
enhanced rate of depolarization and heart rate increases
Parasympathetic Regulation of Heart Rate
oReduces rate of depolarization in SA and AV node through activation of inhibitory
and stimulatory G protein
oACh interacting with cholinergic receptor - in this case, in cells of the heart, they
are muscarinic receptors. AChR is described as muscarinic or nicotinic. In the
heart, it is muscarinic R.
oGet activation of inhibitory and stimulatory G protein.
Inhibitory protein acts to close the T-type Ca++ channels - reduces Ca
current into cell and reduces the depolarization rate.
Stimulatory protein opens K+ channel - K leaves cell, reduces
depolarization and enhances hyperpolarization

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oThese both decrease the rate and magnitude of depolarization - leads to slower
heart rate
Parasympathetic and sympathetic tone to the heart
oPossible to quantify the amount of sympathetic and amount of parasympathetic
using pharmacological measures
oAmount of input is referred to as the TONE
oSolid line = normal situation
oWith sympathetic stimulation, slope of pacemaker potential is enhanced and we
get a faster heart rate due to action of Ca and Na current.
oWith parasympathetic (vagal) stimulation input to heart, it takes a longer time for
pacemaker potential to meet threshold to be met so heart rate slows down
o2 competing inputs into the heart which are always providing some sort of tone to
the heart
oParasympathetic dominates sympathetic 
oparasympathetic (vagal) tone > sympathetic tone
oCan think of parasympathetic as a braking system and sympathetic as an
accelerator. Under normal conditions if pacemaker were allowed to depolarize on
its own, without any input from sympathetic or parasympathetic, it depolarizes at
a rate of 100-110 beats/min. This would be a neutral situation. Have pacemaker
cells depolarizing at this high rate. Unless we are exercising, heart rate isn’t
normally 100 beats a min. usually 60-70 beats/min
oSince normal heart rate is lower than intrinsic rate of depolarization of the
pacemaker cells, this means the pacemaker cells are being slowed under normal
conditions. Vagal tone is having a greater effect than sympathetic tone
Quantification of Parasympathetic and Sympathetic Tone to the Heart
oWe can quantify how much vagal tone and sympathetic tone there is to the heart
through pharmacological agents that are going to block the receptors on the
cardiac cells that are responsible for ACh and NE
oLooking at parasympathetic tone from vagus nerve, ACh is being released onto
heart cells. Type of cholinergic-R is a muscarinic-R. Classical anti-muscarinic
drug that is injected to block muscarinic R is atropine - can block the effects of
parasympathetic nervous system by putting atropine onto heart.
oOn sympathetic nervous side, the majority of action of NE on the heart is through
B-adrenergic R. Adrenergic are alpha or beta. On cardiac contractile cells, Beta-
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