Muscle (smooth/cardiac) Flashcards
(103 cards)
1
Q
What two ways can a muscle contract
A
- isotonically
- isometrically
2
Q
Force generated is sufficient to move load
A
Isotonic (same strength)
3
Q
What can determine the force-velocity relationship?
A
Isotonic contract
4
Q
Force generated is insufficient to move weight placed on muscle (afterload)
A
Isometric contraction (same length)
5
Q
What can determine the length-tension relationship?
A
Isometric contraction (same length)
6
Q
Example of isometric contraction
A
Pressing in door frame
7
Q
Afterload is above maximal force and preload is changed
A
Length-tension relationship
8
Q
What is measured in the length tension relationship?
A
Active force
9
Q
What does the length tension relationship show
A
That stretching a muscle (to a point) can increase force generated
10
Q
Why does stretching a muscle increase force generated?
A
Stretching of a muscle allows cross bridges to form more easily because of betters alignment of actin and myosin fibers
11
Q
How is skeletal muscle already set in terms of preload
A
It is set close to the optimal preload (length)
-bc fixed at both ends mostly
12
Q
What happens when you overstretch a muscle?
A
Lose force generation
13
Q
Preload is set, afterload is changed
A
Isotonic and force-velocity relationship
14
Q
Muscles and afterload
A
Muscle will develop as much force as is needed to lift specific load
15
Q
What does the isotonic and force velocity relationship determine
A
As load increases, the speed at which you lift decreases
- more cross bridges need to form
- slower contraction gives more cross bridges more time to form
16
Q
Given Jame’s diagnosis of Duchenne muscular dystrophy, what would you except if someone experimentally excited the motor neuron to his bicep
A
Normal AP propagation, because the dystrophy is in the muscle, not the nerve
17
Q
What is smooth muscle controlled by
A
Endocrine and ANS
18
Q
Smooth muscle
A
- no conscious control
- can operate effectively when greatly stretched
- fatigue resistant
- generate resting tone-stay partially contracted
19
Q
What are the two types of smooth muscle units
A
Single unit
Multi unit
20
Q
Single unit smooth muscle cells
A
- GI, bladder, uterus
- cells linked by gap junctions
- littler innervation
- some can generate own AP
- all contract together to form own rhythm to expel things
21
Q
Multi unit smooth muscle
A
- Iris, vas deferens
- each cell has its own innervation
- function as distinct muscle cells (like skeletal)
22
Q
Smooth muscle appearance compared to skeletal muscle
A
Smaller than skeletal muscle and spindle shaped, no sarcomeres
23
Q
How are actin and myosin held in place in smooth muscle
A
With dense bodies, intermediate filaments
24
Q
Does smooth muscle have troponin
A
No
Has calponin and caldesmon which are similar
25
What kind of connections do smooth muscle have
Mechanical, can have gap junctions
26
Do smooth muscle have T tubules
No, by they have caveolae whihc function similarly
27
Does smooth muscle have SERCA or SR
Yes, but they don't have a triad configuration
28
E-C coupling in smooth muscle
- extracellular calcium enters cytoplasm
- this releases Ca2+ from SR, whihc binds to calmodulin
- calmodulin activates myosin-light chain kinase (MLCK), which controls cross bridge cycling
29
`how does calcium enter the cytoplasm of the smooth muscle
-depolarization, ligand gated channels, or 2nd messenger gated channels
30
What kind of calcium release is involved in smooth muscle
Calcium induced calcium release
31
What does myosin-light chan kinase (MLCK) do
Phosphorylates myosin light chain
32
Where does the calcium come from for smooth muscle
Some in the SR
| Some from outside
33
Where does the calcium come from for skeletal muscle
ALL Ca2+ from SR
34
Calcium entry through the 2nd messenger gated channels
- hormones of NT activate Gq receptors, which make IP3
- directly open IP3 gate channels on SR
- IP3 dependent Ca2+ opens other Ca2+ channels
35
Calcium enters into smooth muscle via depolarization
- spread through gap junctions, opens VGCC on cell surface
| - this calcium can open RyR channels on the SR to increase calcium more
36
Calcium enters into smooth muscle via ligand gated channels
- hormones and NT open channels and let calcium in
| - this calcium can open RyR channels on SR, can also open VGCCs
37
Cross bridge cycling in smooth muscle
- calcium binds/activates calmodulin
- calmoduling activates MLCK
- MLCK will phosphorylate myosin whihc increases ATPase activity
- cross bridge cycling proceeded as in skeletal muscle as long as myosin is phosphorylated
38
What is myosin de phosphorylates by in smooth muscle
Myosin phosphatase
39
Cross bridging in smooth muscle simplified
Ca2+-calmodulin-MLCK-myosin phosphorylated
40
How does smooth muscle relax?
Dephosphorylation of myosin by myosin phosphatase
- occurs when MLCK is no longer active, requires low ICF Ca2+
- reduces ATPase activity and actin affinity
41
How does smooth muscle contract?
Either physically or tonically
42
Phasic contractions in smooth muscle
Are like skeletal muscle
| -single spike of Ca2+, single contraction, and relaxation
43
Tonic contractions in smooth muscle
- signed Ca2+ spike but maintinaed force
- possible because of the 'latch state" of smooth muscle myosin
- low metabolic demand
44
What is latch state in smooth muscle
- for myosin to let go it has to bind ATP
- unphosphorylatd mysoin has low affinity for ATP
- if it dephosphorylates while still attached to actin, it is slow to release because it is unlikely to bind ATP
45
What does latch state of smooth muscle allow for
Retina muscle tone to be generated at a much lower metabolic cost
46
Why is smooth muscle not striated
No sarcomere
47
Is the cycling of cross bridges slower or faster in smooth muscle compared to striated?
MUCH slower
48
Length of contractions in smooth compared to striated
Longer
49
What type of muscle can "latch"
Smooth
50
What is the metabolic demand on smooth muscle compared to striated
Lower
51
What causes the release of ca2+ in smooth muscle
Extracellular calcium
52
What kind of junctions do smooth muscle have
Gap
53
What is smooth muscle activated by
Circulating hormones or NT
54
Can you overstretched smooth muscle?
Not really because they don't have sarcomeres
55
Length tension relationship of smooth muscle
Given time to accommodate, it will generate maximum force at any length
-same maximal force at all lengths because always have myosin/actin lineup
56
Force velocity relationship of smooth muscle
Increased load increases Ca2+ flux, increases MLCK activation, so it occurs stronger and faster
- velocity of contraction increases with % of myosin phosphorylated
- % phosphorylated increases with load
57
What does force velocity relationship of smooth muscle depend on
Phosphorylation of calcium
58
Muscles that need ECF Ca2+
- cardiac (always) and smooth (depends)
- hypercalcemia (stronger)
- hypocalcemia (weaker)
59
How does ECF calcium alter cell excitability (AP)
By changing threshold of Na(v)
| -this is one instance where presence of Na will affect depolarization
60
Hypercalcemia in smooth muscle and cardiac muscle
Threshold more negative
- less excitable
- Ca2+ likes to keep Na+ channels closed
- contractions strong, but harder to have one
61
Hypocalcemia in smooth and cardiac muscle
Threshold less negative
- more excitable
- easy for muscle to contract but it is a weaker contraction
- test for it by flicking face and seeing if the muscles twitch
62
What would you expect to occur to strength of skeletal muscle contraction in the setting of hypercalcemia
Nothing
63
What would you expect to occur to strength of smooth muscle contraction in the setting of hypercalcemia
Stronger
64
Shape of cardiac muscle cells
Short, Y-shaped, chunky cell
65
What is responsible for the fact that the cardiac muscle contracts as one muscle?
Gap junctions at intercalated disks
| -intrinsic muscle
66
Are APs longer or shorter in cardiac muscle
Longer
67
T-tubules in cardiac muscle
Fewer, but larger
68
Metabolism of cardiac cells
Fatigue resistance, more mitochondria, highly metabolic
69
Proximity of DHPR and RyR in cardiac muscle
Not close, must have extracellular calcium
70
Sarcolemmal calcium pumps in cardiac muscle
There are more of them (NCX and SERCA)
71
Resting membrane potential of cardiac muscle cells
Slightly lower
| -there's more K+ channels here, that's why
72
How many phases are in a cardiac muscle action potential
4
73
Phase 4 of cardiac AP
RMP same as other excitable cells
| -K+ leak channels (iK1)
74
Phase 0 of cardiac muscle AP
```
Upstroke
Na(v) channels open
```
75
Phase 1 of cardiac muscle AP
Early repolarization
| K+ channels i(t0)
76
Phase 2 of cardiac muscle AP
| ***
Plateau
- L-type Ca2+ channels and SR dump
- really long because of all of the calcium that moves
- reduces arrhythmia and tetanus
- needs to fully contract, and fully relax, not go into tetanus, this is why is needs to be this long
77
Phase 3 of cardiac muscle AP
Late repolarization
| -K+ channels i(K)
78
Absolute refractory period of cardiac muscle (ARP)
Much longer
- this prevents tetany
- calcium open for a very long time
- ECF ca2+ is required to open RyR channels on SR, occurs during phase 1 and 2
79
Effective refractory period of cardiac muscle AP
- no conducted potential can generate AP (AP will fire nut not go anywhere)
- can get AP but not from normal source (such as electrodes)
80
Why do doctors want to lengthen the cardiac effective refractory period?
If you lengthen it, it treats arrhythmia. Do it by using K+ channel blockers
81
Relative refractory period (RRP) in cardiac AP
AP can fire if a greater than normal stimulus is provided
| -will have shortened plateau
82
Supra normal period (SNP) in cardiac AP
Cell is more excitable than normal. Has yet to reach full RMP
83
Cardiac muscle mechanical
-contains sarcomeres and cross bridge cycling occurs as in skeletal muscle
84
Force generation in cardiac muscle compared to skeletal
Very slow
- different mysoin isoform, lower ATPase activity
- cardiac muscle needs to fully contract every time (100%), skeletal muscle has to be repeatedly stimulated
85
How do you increase force generation in cardiac muscle
Increasing calcium flow and sensitivity
86
What relationship is muy importante in cardiac muscle
Length tension relationship
87
Length tension relationship in cardiac muscle
Resting length is much shorter than optical length
- heart can generate more force when preload is increased
- it can stretch more than normal which causes much more force
88
What is the length-tension relationship in cardia muscle called
Frank starling law
89
Frank starling law
Length tension relationship in cardiac muscle
| -heart can generate more force when preload is increased
90
What are cardiac pacemakers
Specialized cells in heart
- electrical conduction system
- SA node is primary
- no SR
91
RMP in cardiac pacemakers
Have an unstable RMP, the line is slanted, not straight
92
How do cardiac pacemakers depolarize
At a set rate
93
What is the basis of heart rate
Cardiac pacemakers
94
What phases of cardiac AP does the pacemakers have
4,0,3
95
Phase 4 AP in cardiac pacemakers
- unstable RMP
- i(K) channels slowly close, depolarization
- I(h) (funny channels, i(f)) channels open, Na+ channel, depolarize
- I(ca)T opens, more depolarization
96
What is the funny channel
A Na+ channel on the cardiac pacemaker that opens during phase 4 AP. Unstable RMP because this channel opens up
97
What is the funny channel activated by
Repolarization
98
Phase 0 cardiac pacemakers AP
Firing of AP
- I(ca)L opens
- depolarize
99
Phase 3 of AP in cardiac pacemakers
Repolarization
| -i(K) channels open
100
PNS synapses of SA node
- M2 receptors (Gi)
- increase i(K) flow (hyperpolarize)
- decrease I(h) flow (funny) reduce slope, takes longer to depolarize
- decrease Ca2+ flow (harder to depolarize)
101
What is the total effect of PNS synapses of SA node
Make slow of phase 4 flatter
102
SNS synapses of SA node
Opposite PNS
- B1 receptors (Gs)
- increase I(h) flow (steeper slope) funny
- increase Ca2+ flow
103
What would you expect to happen to SA node depolarization rate (Phase 4) during hypernatremia?
Faster
-funny current open, allows Na+ in
Everywhere, Na+ doesn't effect RMP
