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HOM > Muscle Physiology > Flashcards

Muscle Physiology Flashcards

1
Q

what are muscle tissues derived from?

A

mesoderm

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2
Q

what are the progenitor cells for muscle?

A

myoblasts -> myotubes

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3
Q

what are satellite cells?

A

stem cells that reside on muscle fibres and become activated upon injury to differentiate to generate new muscle fibres and repair skeletal muscle tissue

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4
Q

what happens to satellite cells when muscle is injured?

A

move to site of injury, proliferate and undergo differentiation?

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5
Q

what is muscle degeneration?

A

an inflammatory response - formation of fibrosis, scar tissue develops

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6
Q

which muscle fibres have satellite cells?

A

skeletal

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7
Q

how can cardiac muscle undergo limited repair?

A

stem cells circulating in blood

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8
Q

how many skeletal muscles are there in human body?

A

around 600

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9
Q

what is epimysium?

A

sheath of connective tissue enveloping whole muscle, connecting to tendons

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10
Q

what is the first subdivision of muscle?

A

fascicles

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11
Q

what are fascicles surrounded by?

A

perimysium

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12
Q

what are muscle fibres surrounded by?

A

endomysium/basal lamina

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13
Q

what are myofibrils made of?

A

end-to-end chains of sarcomeres

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14
Q

what are the contractile units of muscle?

A

sarcomeres

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15
Q

what is the basis of the term striated muscle?

A

characteristic banding from sarcomeres

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16
Q

why are the A bands of sarcomeres dark?

A

anisotropic and contain thick filaments

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17
Q

why are the I bands of sarcomeres light?

A

isotropic, contain thin filaments

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18
Q

where are Z lines?

A

in centre of I bands, either end of sarcomeres

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19
Q

where is the M line?

A

centre of A bands, centre of sarcomere

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20
Q

what happens to the respective width of the A and I bands in sarcomeres when muscle contracts?

A

I bands get thinner, A band stays same width

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21
Q

what are the 3 cytoskeletal filaments?

A

actin, microtubules, intermediate filaments

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22
Q

which are the thickest most rigid cytoskeletal filaments?

A

microtubules

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23
Q

what are the key functions of microtubules?

A

acting as tracks for intracellular trafficking, forming mitotic spindle that separates chromosomes during cell division

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24
Q

what are the functions of intermediate filaments?

A

important roles in cell mechanics, maintaining cell structural integrity

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25
Q

what are the functions of actin?

A

key structural polymer, actin networks support cell shape, drive cell deformations in most animal cells.

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26
Q

what is the structure of actin monomers?

A

assemble head to tail to form double helix so actin filament has 2 structurally distinct ends- a plus and a minus

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27
Q

where does active polymerisation occur in non muscle cell actin filaments?

A

at plus ends

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28
Q

where does depolarisation occur in non muscle cell actin filaments?

A

at minus ends

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29
Q

where are the plus ends of actin filaments anchored?

A

at Z-disk

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30
Q

what are the 3 classes of cytoskeletal motors?

A

myosin, dyneins, kinesins

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31
Q

what are cytoskeletal motors?

A

proteins which convert chemical energy of ATP into mechanical energy

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32
Q

which cytoskeletal motors are microtubule based?

A

dyneins and kinesins

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33
Q

what is the function of dyneins?

A

orchestrate transport of cargoes along the axon

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34
Q

what is the function of kinesins?

A

orchestrate transport of cargoes along axon

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35
Q

how many human myosins are there?

A

39

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36
Q

how many classes of human myosins are there?

A

12

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37
Q

what is the function of myosin 6?

A

cargo transport

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38
Q

what is the function of myosin 1?

A

attachment of actin to plasma membrane

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39
Q

what is the function of myosin 2?

A

largest myosin molecules, generate contractility by cross linking and pulling actin filaments

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40
Q

what is the structure of myosin?

A

a hexamer, 2 heavy chains, 2 essential light chains, 2 regulatory light chains

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41
Q

what does each myosin heavy chain contain?

A

actin-binding site, flexible hinge region and long tail region

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42
Q

what are both the heavy and light chains of myosin regulated by?

A

phosphorylation

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43
Q

what is tropomyosin?

A

rod-shaped molecule that forms alpha-helical subunits that become packed into depth of groove that is formed by the actin chains of an actin filament

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44
Q

how many actin units does 1 tropomyosin molecule span?

A

7

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45
Q

what does tropomyosin do in resting skeletal muscle?

A

prevents binding of actin to myosin

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46
Q

what is the function of troponin?

A

moves tropomyosin deeper into the groove to to uncover the myosin binding site on actin

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47
Q

what is alpha-actinin?

A

rod-shaped homodimer of about 35nm in length with an actin binding site on each end

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48
Q

what is the function of alpha-actinin?

A

cross-link actin filaments at the z-disks

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49
Q

what are nebulin and titin?

A

large structural proteins anchored at the Z-disk which contribute to the structural integrity of the sarcomere

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50
Q

what is the role of titin?

A

stabilises myosin thick filaments in the middle of the sarcomere preventing them from deviating too much from the central position

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51
Q

what is the diameter of cardiac muscle cells?

A

up to 10 microns

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52
Q

what is the length of cardiac muscle cells?

A

up to 200 microns in length

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53
Q

which are larger, cardiac or skeletal muscle fibres?

A

skeletal muscle fibres

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54
Q

how are adjacent cardiac cells coupled to each other?

A

mechanically and electrically in a branched and an end-to-end manner by intercalated disks resulting in a syncytium

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55
Q

what do smooth muscle cells line?

A

the walls of hollow organs (gut, airways, blood vessels, urogenital system)

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56
Q

what is the load against which smooth muscle works?

A

the pressure within the tubular structures it lines

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57
Q

how is pressure maintained in organs such as blood vessels?

A

by tonic contraction of smooth muscle

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58
Q

how are contents propelled through tubes such as the gut by smooth muscle?

A

phasic contraction used to propel the contents through the tube

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59
Q

what is smooth muscle better suited to than skeletal muscle?

A

sustained contractions

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60
Q

which contracts/relaxes more slowly, smooth or skeletal muscle?

A

smooth muscle

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61
Q

what are the properties of smooth muscle cells?

A

elongated, often spindle-shaped, much smaller than skeletal muscle fibres

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62
Q

how large are smooth muscle cells?

A

3-5um diameter, up to a few hundred um long

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63
Q

why are smooth muscle cells ‘smooth’?

A

they have no visible striations or sarcomeres in their cytoplasm

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64
Q

how are the actin and myosin filaments of smooth muscle cells arranged?

A

thick myosin and thin actin filaments oriented along length of cell

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65
Q

what are the contractile bundles in smooth muscle cells attached to?

A

dense bodies in the cytoplasm

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66
Q

how are dense bodies in the cytoplasm of smooth muscle cells connected to each other?

A

through intermediate filaments

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67
Q

what are dense bodies connected to in the membrane of smooth muscle cells?

A

attached to adhesion plaques

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68
Q

what are dense bodies in smooth cells analogous to in skeletal muscle cells?

A

Z disks and alpha-actinin

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69
Q

what is the function of dense bodies?

A

act as anchors for filaments to allow efficient shortening of the cell

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70
Q

how are most smooth muscle cells connected?

A

extensive electrically-conducting gap junctions between cells which allows propagation of waves of electrical excitation/intracellular messengers through the tissue

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71
Q

what happens in the cross-bridge cycle?

A

myosin head without bound nucleotide tightly attached to actin filament, ATP binding leads to conformational changes, reduces affinity of myosin for actin, myosin head releases actin filament, myosin head remains very close to actin filament ready to bind again. ATP binding also causes myosin head and neck to pivot into cocked position causing myosin head to move along actin filament. ATP is hydrolysed, ADP and Pi stay bound to myosin. cocked myosin binds actin filament weakly, triggering Pi release, in turn affinity for actin increases. Pi release triggers ‘power stroke’, myosin returns to original conformation, actin filament pulled toward centre of sarcomere, triggers ADP release, return to original state

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72
Q

what causes rigor mortis?

A

when a person dies all ATP rapidly depleted, any myosin attached to actin filament will remain attached until proteins decay

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73
Q

how many ATP molecules are consumed in each cross-bridge cycle for 1 step of a myosin along 1 actin filament?

A

1

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74
Q

how many myosins does each sarcomere filament have?

A

around 300

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75
Q

how many sarcomeres can large muscles like biceps contain?

A

100,000

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76
Q

what is the ATP in a cell enough for?

A

around 8 twitches

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77
Q

what does creatinine phosphate do?

A

provides intracellular backup system that can provide enough ATP for around 100 twitches

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78
Q

what are used to produce ATP at increased exercise activity?

A

aerobic and anaerobic mechanisms that mostly use glucose as a substrate

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79
Q

what is the role of calcium in skeletal and cardiac muscle contractility?

A

regulates binding of myosin to actin via tropomyosin and troponin

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80
Q

what are the 3 subunits of skeletal muscle?

A

TnI (inhibitory), TnC (calcium ions), TnT (tropomyosin)

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81
Q

what happens to skeletal muscle troponin when intracellular calcium increases?

A

TnC binds up to 4 calcium ions, leads to conformational change which causes TnI to release its hold on actin, tropomyosin displaced deeper in actin double helix groove so myosin-binding sites become accessible

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82
Q

what is the difference between activation of contraction by calcium in cardiac vs skeletal muscle?

A

cardiac TnC binds 3 calcium ions not 4

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83
Q

what is the main activation mechanism of smooth muscle contraction?

A

every myosin molecule has 2 regulatory light chains (Myosin Regulatory Light Chains) regulated by phosphorylation, leads to activation of myosin activity through conformational change enhancing actin binding and increase in ATPase activity

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84
Q

how is MRLC phosphorylation controlled in smooth muscle?

A

intracellular calcium through regulatory protein calmodulin

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85
Q

what is calmodulin closely related to?

A

TnC (calcium binding subunit of troponin)

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86
Q

what happens when calmodulin binds calcium?

A

Ca-CaM complex activates kinase MLK, phosphorylates MRLCs

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87
Q

how long can maximal contraction take to occur in smooth muscle?

A

up to 1s

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88
Q

how much slower is ATP hydrolysis in the cross-bridge cycle than in skeletal myosins?

A

10x slower

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89
Q

what does intracellular calcium decrease lead to in skeletal and cardiac muscle?

A

termination of contraction

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90
Q

what is needed for termination of contraction in smooth muscle?

A

intracellular calcium decrease AND MRLC dephosphorylation

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91
Q

what mediates MRLC dephosphorylation?

A

myosin light chain phosphatase (MLCP)

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92
Q

what does experimental evidence suggest happens in MRLC dephosphorylation occurs when myosin is bound to the actin filament?

A

myosin remains bound with a high affinity - cross-bridges in this state are latch bridges

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93
Q

what do latch bridges allow?

A

maintenance of tension without cross-bridge cycling or ATP consumption

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94
Q

why is smooth muscle up to 300x more efficient than skeletal during maintained contractions?

A

latch bridges formed by MRLC dephosphorylation while myosin is bound to actin

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95
Q

what proteins regulate contraction at the actin filament level in smooth muscle?

A

caldesmon and calponin

96
Q

what do caldesmon and calponin do?

A

bind actin and smooth muscle tropomyosin and inhibit interaction between actin and myosin

97
Q

what binds caldesmon and calponin and what does this do?

A

Ca-CaM complex, relieves their inhibitory effects on actin-myosin binding

98
Q

what are muscle dystrophies?

A

inherited conditions resulting in disorganisation of the myofilaments and eventual paralysis

99
Q

what proteins are some muscle dystrophies associated with?

A

titin and dystrophin

100
Q

what does dystrophin do?

A

connects the actin thin filaments to the extracellular matrix

101
Q

what is the extracellular matrix in muscle fibres?

A

network of elastic filaments that surrounds the muscle fibres

102
Q

what is Duchenne muscular dystrophy?

A

a rare genetic X-linked recessive condition which results from mutations disrupting dystrophin

103
Q

what happens to muscles in the absence of dystrophin?

A

they are easily damaged damage accumulates resulting in general muscle weakening over time

104
Q

what are hypertrophic cardiomyopathies?

A

an inherited condition characterised by thickening of ventricular walls and a smaller ventricular chamber

105
Q

what are many HCMs caused by?

A

a single mutation in cardiac beta myosin heavy chain

106
Q

what is a motor unit?

A

set of all muscle fibres innervated by 1 presynaptic neuron

107
Q

what is tone?

A

low level of activity shown by small motor units at rest

108
Q

what produces muscle tone?

A

stretch reflex from muscle spindle receptors

109
Q

what is tone responsible for at rest?

A

firmness of muscles

110
Q

what is poliomyelitis?

A

a disease which destroys motor axons

111
Q

where is acetylcholinesterase found?

A

in membrane in synaptic cleft

112
Q

what is the structure of NAChRs?

A

pentameric molecule, central cation channel, ligand-gated. 2 binding sites for ACh

113
Q

how many ACh binding sites do NAChRs have?

A

2, both must be bound for cation channel to open

114
Q

when does the NAChR become desensitised?

A

if ACh levels high for a long time

115
Q

what is the NAChR channel permeable to?

A

sodium and potassium ions and calcium a little bit

116
Q

when does the graph cross the x-axis if plot inward flux of positive current and outward flux of positive current against membrane potential in postsynaptic membrane?

A

near 0

117
Q

what is seen in EPPs in curare-treated muscle when they are too small to trigger action potentials?

A

peak size of EPPs decays exponentially with distance from endplate because more endplate current leaks to outside across muscle fibre membrane

118
Q

what is the difference in selectivity of the 4 calcium binding sites in skeletal muscle?

A

2 are more selective for Ca2+ than Mg2+

119
Q

what does a muscle AP trigger from the sarcoplasmic reticulum?

A

Ca2+ release

120
Q

why is the transverse (T) tubular system required?

A

to carry surface excitation deep into skeletal muscle fibre to allow uniform, rapid Ca2+ release across entire cross-section of each fibre

121
Q

what is the T tubular system?

A

invaginations of membrane which penetrate into interior of muscle fibre, lumen continuous with extracellular space

122
Q

what increase in SA does the T tubular system cause?

A

6-10 times greater

123
Q

what is each individual myofibril in skeletal muscle surrounded by?

A

a T tubule

124
Q

where do T-system networks occur in the sarcomere in mammalian skeletal muscle?

A

at junctions between A and I bands

125
Q

where do T-system networks occur in the sarcomere in mammalian cardiac and frog skeletal muscle?

A

at the Z line

126
Q

when can local surface depolarisation of muscle fibre using a fine micropipette produce contraction of underlying sarcomeres?

A

if micropipette located precisely on external opening of T-tubules

127
Q

what system does the SR form?

A

longitudinal system of tubules and sacs which come into close contact with T-tubules at terminal cisternae

128
Q

where does the SR come into close contact with T-tubules?

A

at terminal cisternae

129
Q

what is the arrangement of cisternae and T-tubules?

A

triad arrangement- 2 terminal cisternae sandwiching transverse tubule to give rise to triad arrangement

130
Q

how do muscle APs propagate into T-tubular system?

A

as along a nerve- allowing efficient, rapid propagation of excitation into fibre

131
Q

how do VGNaCs amplify depolarisation of the T-system membrane?

A

conduction of Na+ ions from T-system into fibre

132
Q

how do VGKCs repolarise the T-system membrane?

A

by conducting K+ from fibre into T-system

133
Q

how is the magnitude of the equilibrium potential for K+ across the T-system membrane reduced over the course of a few APs?

A

T-system volume less than 0.5% of the whole cell volume so K+ can build up in T system, reduces magnitude of equilibrium potential

134
Q

why is the T-system more permeable to Cl- than K+ at rest?

A

due to Clc1 chloride channels

135
Q

why does Cl- tend to keep membrane potential of the T-system well-polarised at rest?

A

Cl- is passively distributed so equilibrium potential of Cl- is similar to resting membrane potential

136
Q

what are DHPRs?

A

voltage sensors (L-type calcium channels) in membrane of T-tubules

137
Q

what are DHPRs mechanically linked to?

A

calcium release channels called ryanodine receptors in SR of skeletal muscle

138
Q

what does depolarisation of T-tubular membrane cause in DHPRs?

A

conformational change , causes conformational change in sarcoplasmic reticulum ryanodine receptor calcium channels which causes them to open

139
Q

how is calcium concentrated in the sarcoplasmic reticulum?

A

by ATP-consuming calcium pumps (SERCA pumps)

140
Q

what is the function of calsequestrin?

A

binds Ca2+ in the SR, reduces the gradient against which SERCA pumps have to work

141
Q

what does opening of ryanodine receptors allow?

A

Ca2+ to flow out of SR down electrochemical gradient to raise conc. within muscle fibre cytoplasm, Ca2+ binds to TnC initiating contraction

142
Q

how are calcium levels in the sarcoplasm reduced leading to relaxation of muscle?

A

calcium is resequestered in sarcoplasmic reticulum by calcium pumps

143
Q

what is force exerted by a muscle more commonly referred to?

A

tension

144
Q

what is the amount of work done a product of?

A

force and distance

145
Q

what is power?

A

the rate of doing work

146
Q

what direction do crossbridges on each half of a filament work in?

A

parallel

147
Q

what is the tension developed by a thick filament the sum of?

A

the tension developed by its individual crossbridges at 1 end

148
Q

how do length changes in series combine?

A

add together

149
Q

why is the tension developed in each myofibril the same as in each single sarcomere in the chain?

A

the sarcomeres are in series

150
Q

what is the maximal force developed by a whole muscle proportional to?

A

the total number of thick filaments in a cross-section

151
Q

what is the effect of lengthening a muscle by adding more sarcomeres in series?

A

increases the total distance of shortening proportionally

152
Q

what is the force of 1 myofibril?

A

number of thick filaments per sarcomere x force of 1 thick filament

153
Q

what is the total muscle force?

A

number of thick filaments x force of 1 thick filament x myofibrils in whole muscle

154
Q

what is total muscle length change?

A

sarcomeres per myofibrils x length change of 1 sarcomere

155
Q

what is the effect of making muscle fatter?

A

increases muscle force

156
Q

what is the effect of making muscle longer?

A

increases muscle contraction velocity

157
Q

what is isometric contraction?

A

contraction of a muscle at constant length

158
Q

what is isomeric tension the sum of?

A

passive tension due to elasticity of connective tissue and cytoskeleton in muscle; active tension due to operation of contractile apparatus

159
Q

what is isotonic contraction?

A

contraction of a muscle under constant load

160
Q

how is isometric tension measured?

A

isometric contraction at different lengths of muscle

161
Q

what does the isometric length-tension relationship of a muscle show?

A

maximal tension developed over a narrow range of lengths corresponding to physiological working range

162
Q

how is active tension calculated?

A

total tension - passive tension

163
Q

when is maximal force developed in a sarcomere?

A

when all crossbridges engaged on thin filament, but opposing thin filaments don’t overlap

164
Q

what reduces crossbridge efficiency in a single sarcomere?

A

collision of thin filaments as sarcomere shortens, then thick filaments colliding with Z discs

165
Q

what is isotonic contraction?

A

contraction of muscle at constant tension

166
Q

what is the relationship between velocity and load in muscle contraction?

A

inverse

167
Q

what is a twitch?

A

the whole mechanical response to a single action potential

168
Q

what is tetanus?

A

sustained contraction

169
Q

what produces tetanus?

A

frequency of action potentials above a certain value producing a constant maximal occupation of TnC by calcium

170
Q

what is the arrangement of myofibrils in a straight strap muscle?

A

aligned parallel to axis of contraction of whole muscle

171
Q

what is the arrangement of myofibrils in pennate and triangular muscle?

A

myofibrils at an angle to axis of bone- can increase total force generating capacity by allowing for more muscle fibre to be attached to the bone

172
Q

what is the parallel elastic element of muscle?

A

elasticity of the relaxed muscle due to membranes and other connective tissue in parallel with myofibrils

173
Q

what is the series elastic element of muscle?

A

springiness of material in series with sarcomeres (tendons, terminal connective tissue, z disks) and elasticity of crossbridges and filaments

174
Q

diameter of slow oxidative muscle?

A

small

175
Q

force/area of slow oxidative muscle?

A

low

176
Q

Vmax of slow oxidative muscle?

A

low

177
Q

myosin heavy chain in slow oxidative muscle?

A

MHC-1

178
Q

diameter of fast oxidative muscle?

A

medium

179
Q

what is type 1 muscle?

A

slow oxidative

180
Q

what is type 2a muscle?

A

fast oxidative

181
Q

what is type 2b muscle?

A

fast glycolytic

182
Q

force/area of fast oxidative muscle?

A

medium

183
Q

Vmax of fast oxidative muscle?

A

medium

184
Q

myosin heavy chain of fast oxidative muscle?

A

MHC-2a

185
Q

diameter of fast glycolytic muscle?

A

large

186
Q

force/area of fast glycolytic muscle?

A

high

187
Q

Vmax of fast glycolytic muscle?

A

high

188
Q

myosin heavy chain in fast glycolytic muscle?

A

MHC-2b

189
Q

fatigue resistance of slow oxidative muscle?

A

high

190
Q

fatigue resistance of fast oxidative muscle?

A

medium

191
Q

fatigue resistance of fast glycolytic muscle?

A

low

192
Q

mitochondria in slow oxidative muscle?

A

a lot

193
Q

mitochondria in fast oxidative muscle?

A

a lot

194
Q

mitochondria in fast glycolytic muscle?

A

few

195
Q

oxidative capacity of oxidative muscle (fast and slow)?

A

high

196
Q

oxidative capacity of fast glycolytic muscle?

A

low

197
Q

glycolytic enzymes in slow oxidative muscle?

A

low

198
Q

glycolytic enzymes in fast oxidative muscle

A

medium

199
Q

example of fast glycolytic muscle?

A

chicken breast gastrocnemius

200
Q

example of fast oxidative muscle?

A

pigeon breast

201
Q

example of slow oxidative muscle?

A

human soleus

202
Q

glycolytic enzymes in fast glycolytic muscle?

A

high

203
Q

how does electrical signal propagate from 1 cardiac cell to another?

A

through gap junctions

204
Q

where is the cardiac activity that controls heart contractions initiated?

A

in the heart independently of nervous system

205
Q

how is cardiac action potential initiated in the normal heart?

A

in sinoatrial node by specialised cardiac myocytes with pacemaker activity

206
Q

what is the primary function of cardiac myocytes in the SAN?

A

generation and conduction of pacemaker potential

207
Q

what is the difference between myocytes in the SAN and atrial/ventricular myocytes?

A

SAN myocytes have fewer myofibres and mitochondria and smaller SR

208
Q

how many times/min does the SA node fire?

A

60-80

209
Q

what is the electrical connection between atria and ventricles?

A

atrioventricular node

210
Q

what electrically isolates the atria and ventricles from each other except for at the AVN?

A

a fibrous AV ring

211
Q

what creates delay in contraction spreading to the ventricles?

A

conduction through AV node is slower than surrounding muscle tissue

212
Q

where does the electrical signal propagate from the AC node?

A

Bundle of His and Purkinje fibres- specialised myocardial cells that act as conducting tissue

213
Q

what is the main function of the bundle of His and Purkinje fibres?

A

conducting electrical signal rather than contraction

214
Q

where does electrical signal propagate from Purkinje fibres?

A

fibres split into 2 branches, propagates into the 2 ventricles

215
Q

what ensures ventricles contract from apex to base?

A

fibre arrangement and speed of signal propagation

216
Q

what is phase 0 of an AP in cardiac myocytes?

A

rapid depolarisation phase

217
Q

what is phase 1 of an AP in cardiac myocytes?

A

initial brief rapid depolarisation

218
Q

what is phase 2 of an AP in cardiac myocytes?

A

plateau

219
Q

what is phase 3 of an AP in cardiac myocytes?

A

terminal repolarisation restores membrane potential to resting level

220
Q

what is phase 4 of an AP in cardiac myocytes?

A

electrical diastole- heart waiting for another electrical trigger to restart the cycle

221
Q

what causes the rapid depolarisation in phase 0 of ventricular muscle cells?

A

voltage gated Na+ channels activated, slower opening of Ca2+ channels

222
Q

what causes the initial rapid repolarisation in phase 1 of ventricular muscle cells?

A

Na+ channels close into inactive state, K+ channels open

223
Q

what causes the plateau in 2 of ventricular muscle cells?

A

Ca2+ channels not inactivated, remain open, Ca2+ influx more or less balances K+ efflux. Ca2+ channels are L-type voltage gated DHPRs, sensitive to calcium blockers which inhibit plateau calcium current

224
Q

what causes the terminal repolarisation in phase 3 of ventricular muscle cells?

A

delayed activation of K+ channels leading to repolarisation

225
Q

what causes the electrical diastole in phase 4 of ventricular muscle cells?

A

membrane returns to resting potential

226
Q

why do cardiac myocytes have long refractory period?

A

AP remains high through plateau phase so Na+ channels stay inactive through that phase- ensures summation and tetanus don’t occur

227
Q

what is the most important feature of APs in SAN cells?

A

SAN cells don’t have true RP as membrane potential always changing so don’t depolarise as much as other cells

228
Q

what is the current due to in SAN cell APs?

A

non-specific cation channel (HCN channel) which has mixed permeability for both Na+ and K+

229
Q

why is the current in SAN APs called the ‘funny’ current?

A

HCN channel has unusual property of opening upon hyperpolarisation

230
Q

when do HCN channels open in SAN APs?

A

at end of phase 3 depolarisation, leads to inward cation current driving slow membrane depolarisation in phase 4

231
Q

how can most intrinsic mechanisms that regulate heart function be modulated?

A

autonomic impulses from sympathetic and parasympathetic nervous systems, indirectly through circulating levels of epinephrine released into blood

232
Q

how does vagal stimulation through ACh slow heart rate?

A

increase in membrane potassium conductance which hyperpolarises membrane of SA by decreasing If, which decreases slope of Phase 4 depolarisation

233
Q

how do sympathetic transmitters norepinephrine and epinephrine increase heart rate?

A

increase If and reduce phase 3 repolarisation, results in increased heart rate. leads to higher but shorter plateau in ventricular cells- stronger contraction

234
Q

how does the T-tubule system work in cardiac myocytes?

A

Ca2+ released through Calcium Induced Calcium Release- Ryanodine receptors activated by extracellular Ca2+ that enters through DHPRs rather than mechanical coupling with DHPRs

235
Q

what are the consequences of calcium induced calcium release?

A

risk of Ca2+ overload, so needs sarcolemmal Na+/Ca2+ exchanger. Ca2+ also re-sequestered in SR between APs. Ca2+ controlled by SERCA pump inhibited by Phospholamban (PLN). amount of extracellular Ca2+ influences how much Ca2+ released from SR

236
Q

what mediates PLN phosphorylation to stop its inhibition of SERCA?

A

PKA as a result of epinephrine signalling

HOM (9 decks)

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