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physiology > Cellular Physiology of Skeletal, Cardiac, and Smooth Muscle > Flashcards

Cellular Physiology of Skeletal, Cardiac, and Smooth Muscle Flashcards

1
Q

What kind of muscles control breathing

A

skeletal, via contraction of the diaphragm and functions as a pump assisting return of the venous blood supply to the heart.

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2
Q

What is the smallest CONTRACTILE unit of skeletal muscle, and one or more nucleas?

A

multinucleated, elongated cell called a muscle fiber or myofiber

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3
Q

what is a fascicle?

A

bundle of linear aligned muscle fibers

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4
Q

what is the epimysium?

A

external sheet that contains the whole muscle.

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5
Q

what is the perimysium?

A

the sheath surrounding the fascicles

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6
Q

what is the endomysium?

A

the sheath surrounding muscle fibers.

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7
Q

what is the sarcolemma?

A

plasma membrane of the muscle cell under endomysium.

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8
Q

what are myofibrils?

A

densely arranged parallel array of cylindrical elements in skeletal muscle cell

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9
Q

what do myofibril consist of?

A

end-to-end chain of regular repeating units—or sarcomeres —that consist of smaller interdigitating filaments called myofilaments;

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10
Q

what do myofilaments consist of?

A

Thick and thin filaments.

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11
Q

where a the cell bodies of somatic neurons found

A

central nervous system ventral horn spinal cord.

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12
Q

what are motor neurons

A

the neurons that control skeletal mucle

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13
Q

what is the innervation ratio of whole skeletal muscle?

A

the number of muscle fibers innervated by a single motor neuron.

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14
Q

what do muscle control with a small innervation ratio

A

fine movements

large ratio= large force movements

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15
Q

Do skeletal muscles use chemcal or electrical activasion?

A

artifical both

otherwise always chemical and ACh

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16
Q

where to AP penetrate the muscle fibers?

A

at the T tubules

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17
Q

at what places do t tubules surround myofibril

A

junction of the A-I bands

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18
Q

what are terminal citsernae?

A

specialized regions of the sarcoplasmic reticulum. where the t tubule associates with (2x)

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19
Q

what is the triad junction

A

. The combination of the T-tubule membrane and its two neighboring cisternae (SR) is called a triad junction, or simply a triad.

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20
Q

The ultimate intracellular signal that triggers and sustains contraction of skeletal muscle cells is a rise in ?

A

[Ca 2+ ] i

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21
Q

what is Excitation-contraction coupling? EC coupling

A

he process by which electrical “excitation” of the surface membrane triggers an increase of [Ca 2+ ] i in muscle

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22
Q

how are L type Ca2+ channels activated

A

voltage gated, in the triad region t Tubule

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23
Q

what is the voltage sensor EC?

A

tetrads (groups of four) of L type Ca2+ channels

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24
Q

what is Cav1.1

A

a α 1 -subunit of the voltage-gated Ca 2+ channel

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25
Q

what is a DHP receptor and why

A 
L-type Ca 2+ channel
because it is inhibited by a class of antihypertensive and antiarrhythmic drugs known as dihydropyridines or calcium channel blockers.
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26
Q

what do l-type ca2+ channels consist of?

A

α1, α2 -δ, β, and γ subunits

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27
Q

what activates the Ca2+ release channel?

A

he voltage-driven conformational changes in the four Cav1.1 channels mechanically activate each of the four directly coupled subunits

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28
Q

what and why is a channels called ryanodine receptor (RYR)?

A

The SR Ca 2+ -release channel, because it is inhibited by the plant alkaloid ryanodine.

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29
Q

what activates the ryonade receptor

A

Caffeine, increasing open probability.

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30
Q

What are the largest channel proteins?

A

RYR

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31
Q

Are there more RYR1 or Cav1.1 channels at the triad?

A

2x as much RYR channels

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32
Q

What underlies EC coupling in the skeletal muscle

A

mechanical interaction between Cav1.1 and RYR channels

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33
Q

what is a spark

A

the rapid rise in local [Ca 2+ ] i from RYR channels

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34
Q

What are thick myofilaments composed of?

A

myosin

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35
Q

what are thin myofilemaments composed of?

A

largely of actin

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36
Q

what is responsible fore the striated appearance?

A

highly organised sacromers

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37
Q

what is a sacromere

A

repeating unit between z discs

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38
Q

to what are thin filaments attached?

A

z-disks

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39
Q

what are z-disks made of?

A

a-actinin

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40
Q

where a titin and nebulin attached to

A

z-disk

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41
Q

what is the role of Z-discs

A

protein organising and tension bearing role.

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42
Q

what are I bands

A

regions where thin filaments dont overlap thick filaments (isoptropic)

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43
Q

what are A-bands

A

Regions where myosin filaments are present

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44
Q

Do a and I bands change in length

A

during contraction, the I bands (nonoverlapping region of actin) shorten, while the A bands (myosin) do not change in length.

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45
Q

out of what does troponin consist

A

troponin T- bind to a single tropomyosin
troponin C- which binds to Ca2+
troponoin I- which binds to actin and inhibits contraction.

46
Q

to what is calmodulin related?

A

troponion C (tnC)

47
Q

do how many actin monomers does tropomyosin bind?

A

7

48
Q

by what is thick filament in fast skeletal muscles assembled?

A

several hundred myosin II

49
Q

what does find place on the myosin heavy chain?

A

binding and hydrolyzing of ATP

50
Q

wgat do the essential light chain and regulatory light chain do?

A

bind to and mechanically stabilize the α-helical neck region

51
Q

what does phosphorylation of the regulatory light chain do.

A

enhances myosin cross-bridge interactions.

52
Q

what does myosin light-chain kinas­es (MLCKs) do

A

phosphorylation of RLF

53
Q

wat doet fosfatase?

A

oposite of (MLCKs) (dus minder cross bridge interactie)

54
Q

what does a rise of Ca2+ i do to troponin

A

Tnt pulls tropomyosin and TnI out the way so that myosin can now interact with actin.

55
Q

what is the largest known protein?

A

titin

56
Q

what is the elastic filament of sacromers?

A

titin

57
Q

what does nebulin do

A

. Nebulin interacts with actin and controls the length of the thin filament; it also appears to function in sarcomere assembly by contributing to the structural integrity of myofibrils.

58
Q

what parts of titin are tethered to what

A

N-terminus to z disk

C terminus to M line

59
Q

What is rigor mortis

A

after death, the lack of ATP prevents the cycle from proceeding further;

60
Q

what does the binding of ATP to the MHC cause?

A

reduces affinity of myosin for actin (causes myosin head to release for actin filament (muscle relaxed)

61
Q

What happens when ATP hydrolises (1st)

A

the myosin head/neck picots into a cocked position, this caused the myosin to line up with a new actin monomere (2 monomers farther along the actin filament ) (muscle relaxed) myosin to their resting conformation.)

62
Q

what happens after ATP hydrolises (2nd)

A

weak cross bridge formation

63
Q

what does the relsease of Pi from myosin cause?

A

increased affinity of the myosin-ADP complex for actin. Strong cross bridge

64
Q

what is the rate-limiting step in croos-bridge cycle?

A

transition from weak to strong, release Pi

65
Q

what does the relsease of Pi from myosin cause? (2nd)

A

conformational change in the myosin head, causes the power stroke. * filament slide pass each other.

66
Q

does the sacromeer get bigger or smaller with release of Pi

A

smaller, Z- lines are pulled together with power stroke.

67
Q

What does the release of ADP cause in cross bridge cycle

A

completes cycle, and the actomyosin complex is left in a rigif, attached state. The relative positions of the actin versus the myosin head, neck, and rod remain the same until another ATP molecule binds and initiates another cycle (step 1).

68
Q

does [ATP]i regulate the cross bridge cycle of actin myosin interaction?

A

no, [Ca 2+ ]i causes temporal control of the cycle.

69
Q

How many Ca2+ binding sites does a skeletal troponin C have?

A

2 pairs

70
Q

is there always Ca2+ or Mg on TNNC2 (skeletal TnC)

A

Two high-affinity sites—located on the C-lobe of TNNC2—are always occupied by Ca 2+ or Mg 2+ under physiological conditions.

71
Q

What is a feature of the N-lobe of TNNC2?

A

two low-affinity sites—located on the N-lobe of TNNC2—bind and release Ca 2+ as [Ca 2+ ] i rises and falls

72
Q

When does the C lobe of TnC interact/ bind to TnI, what does that cause?

A

at high [Ca 2+ ] i ,to cause tropomyosin to translocate by 25 degrees on the F-actin surface, which allows the cocked myosin head group to interact weakly with actin

73
Q

where does Ca2+ be removed to end contraction

A

sacroplasm

74
Q

What is NCX

A

Na-Ca exchanger

75
Q

what is PMCA

A

plasma memrbane Ca-ATpase or pump

76
Q

How is Ca2+ extruded from the sacroplasm?

A

NCX (Na-Ca exchanger)
PMCA (plasma membrane Ca-ATPase or pump)
in SR, by SERCA ((sarcoplasmic and endoplasmic reticulum Ca-ATPase or pump)

77
Q

what is the most important mechanism od extruding Ca2 from sacroplasm and why

A

SERC ((sarcoplasmic and endoplasmic reticulum Ca-ATPase or pump, otherwise the cell would completely be depleted from Ca2+

78
Q

What is SERCA

A

(sarcoplasmic and endoplasmic reticulum Ca-ATPase or pump) 2 Ca (+ ATP) in SR 2 H+ out

79
Q

what inhibits SERCA

A

high Ca2+ in SR lumen

80
Q

How does the SR keep its [Ca 2+ ] high and store a lot +names

A

by binding proteins.
casequestin (CSQ)
and calreticulin

81
Q

what is difference between Calreticulin and calsequestrin

A

calsequestrin mostly in skeletal and cardiac (some smooth_ calreticulin mostly in the SR of smooth muscle.

82
Q

how many binding sites do Calreticulin and calsequestrin have

A

50

83
Q

what deactivates RYR

A

dissociation of Ca from CSQ calsequestrin

84
Q

where is CSQ mostly found in SR and what does it accoaite with

A

highly localized to the region of the SR immediately beneath the triad junction, where it forms a complex with the Ca 2+ -release channel and with two other RYR-anchoring proteins—junctin and triadi

85
Q

what are triadin and junctin

A

RYR anchoring proteins

86
Q

what are isometric contractions

A

stimulation that causes an increase in tension but no shortening

87
Q

what are isotonic contractions?

A

stimulation causes shortening

88
Q

what is passive tension

A

The tension measured before muscle contractio

89
Q

what is active tension

A

the additional tension at any fixed length developed by cross-bridge cycling

90
Q

what is the total measured tension?

A

he sum of the passive and active tension.

91
Q

what is the optimal length

A

active tension maximum, near normal muscle length

92
Q

when is active tension maximum regarrd to length

A

near normal muscle length, so decreases when muscle is smaller or larger (isometric

93
Q

This length-tension relationship is a direct result of the anatomy of the thick and thin filaments within individual sarcomeres explain why

A

the ends of the actin filaments are pulled beyond the ends of the myosin filaments. Under this condition, no interaction occurs between actin and myosin filaments and hence no active tension develops.As the muscle shortens further, opposing actin filaments slide over one another and the ends of the myosin filaments and—with extreme degrees of shortening—eventually butt up against the opposing Z disks. Under these conditions, the spatial relationship between actin and myosin is distorted and active tension falls. .

94
Q

Note that for isotonic contractions, the applied load is … the tension in the muscle.

A

Note that for isotonic contractions, the applied load is the same as the tension in the muscle.

95
Q

what explains that all initial muscles lengths have same initial maximal velocity at zero load.

A

it depends on the maximal rate of cross-bridge turnover, not the initial overlap of thin and thick filaments.

96
Q

where is Power maximum?

A

t intermediate loads (where both F and v are moderate) and falls to zero at maximum load (where v = 0) and at zero load (where F = 0).

97
Q

Is it possible to fire a new AP before contraction is experired

A

yes, because the muscle twitch far exceeds the duration of the action potential

98
Q

What is summation

A

the second action potential stimulates a twitch that is superimposed on the residual tension of the first twitch and thereby achieves greater isometric tension than the first

99
Q

what happens to the tension if the frequency of the AP are grouped closer in time

A

increases

100
Q

what is frequency summation?

A

tension enhancement depends on the frequency of muscle stimulation

101
Q

What is tetanus (twitches)

A

the sate in which individual twitches are no longer distinguishable from each other (fused)

102
Q

what is needed for [Ca 2+ ] i in order to achieve tetanus

A

nu sufficient time for [Ca 2+ ] i to lower to a level that initiates relaxation

103
Q

what happens to tension at stimulation frequencies above fusion frequency?

A

tension increases very little.

104
Q

what is mulitple fiber summation?

A

ach additional motor-neuron cell body within the spinal cord is excited, those muscle fibers that are part of the motor unit of that motor neuron are added to the contracting pool of fibers

105
Q

are smaller or bigger motor units recruited with minimal neuronal stimulation and why?

A

smaller, Because a given excitatory stimulus will generate a larger excitatory post­synaptic potential in motor neurons with smaller cell bodies

106
Q

what is the size principle

A

he progressive recruitment of first small and then larger and larger motor units

107
Q

what us motor neuron pool

A

The group of all motor neurons innervating a single muscle

108
Q

what is spatial summation?

A

Multiple-fiber summation,ach additional motor-neuron cell body within the spinal cord is excited, those muscle fibers that are part of the motor unit of that motor neuron are added to the contracting pool of fibers

109
Q

what is essential for fine motor control

A

smooth nontetanic contractioon

110
Q

why does the CNS activate individual motor units asynchronously so that some units are developing tension while others are relaxing. .

A

so the whole muscle force can be relatively constant with time, even when individual fibers are not stimulated to tetanus

physiology (8 decks)

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