Term
| What is the structure of smooth muscle? |
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Definition
Actin filaments radiate from dense bodies; ends overlapping myosin filaments interspersed in between actin
Dense bodies attached to one another by intracellular protein bridges; serve as “Z disks”
Lacks troponin complex, not striated |
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Term
| Explain multiunit smooth muscle |
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Definition
There is an electrical isolation of cells as each cell has its own neuron and synaptic contact
Each fiber can contract independently
Location - Iris, ciliary muscles of eye, vas deferens, piloerector muscles
Action potentials not common - fibers too small and not coordinated
ANS stimulation in the varicosities (synaptic contacts) caused by ACh and or NE
Cause a local depolarization (“junctional potential”) which spreads over fibers causing contraction |
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Term
| Explain unitary smooth muscle |
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Definition
One synaptic contact and gap junctions spread the impulse allowing for coordinated contraction as a single unit
location - GI tract, bile ducts, bladder, ureters, uterus, blood vessels
Action potentials normally occur; 30-40 muscle fibers must depolarize simultaneously before AP occurs |
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Term
| What are the three types of smooth muscle action potentials? |
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Definition
typical spike AP - elicited by an external stimulus (electrical stimulation, hormones, stretch, spontaneously)
plateau AP - allows for prolonged contraction, occurs in uterus, ureter, vascular smooth muscle
Slow waves (pacemaker waves) – low oscillation of RMP- do not reach threshold unless strong enough - if slow wave potential reaches threshold (~ -35 mV) - trains of action potentials are generated – rhythmical contraction
Slow waves aren't AP's but generate AP's. They are controlled by the interstitial cells of Cajal |
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Term
| What is the sequence of excitation-contraction coupling in smooth muscle? |
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Definition
1) action potential in smooth muscle membrane
2) opening of voltage-sensitive Ca2+ channels
3) ICF levels of Ca2+ rise (due mostly to Ca2+ from the ECF and only a little from SR)
4) Ca2+ binds to calmodulin and activates it
5) Ca2+-calmodulin binds to myosin light chain kinase and activates it
6) Myosin is phosphorylated and forms the cross-bridge with actin
7) dephosphorylation of myosin causes latch-bridge formation |
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Term
| What is latch-bridge formation? |
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Definition
In smooth muscle even when Ca2+ levels are low myosin and actin don't detach or detach very slowly. It is caused by dephosphorylation of myosin
This is a called a latch-bridge formation and it causes tonic tension |
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Term
| Compare phasic and tonic contraction |
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Definition
Phasic contraction is twitch-like shortening followed by relaxation
Tonic contraction is where the force is sustained for very long periods.
The ability to maintain force of contraction with decreased numbers of activated crossbridges greatly reduces the amount of energy consumption (ATP turnover) |
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Term
| What are the different ways to increase ICF levels of Ca2+ in smooth muscle? |
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Definition
1. Voltage-gated Ca+2 channels – opens with AP depolarization
2. Ligand-gated Ca+2 channels – receptor-mediated; hormones/neurotransmitters
3. IP3- gated SR Ca+2 channels – receptor mediated;
hormones/neurotransmitters
4. Leak channels |
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Term
| What are the different ways to decrease ICF levels of Ca2+ in smooth muscle? |
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Definition
Ca2+/Na+ exchanger - counter-transporter
CaATPases at the plasma membrane and the sarcoplasmic reticulum
These pumps are slower in smooth muscle than in skeletal muscle |
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Term
| What is Raynaud's phenomenon? |
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Definition
Skin discoloration due to abnormal spasm of vascular smooth muscle in peripheral tissues causing a diminished blood supply to local tissues
Skin discoloration upon temperature or emotional changes: initially, digit(s) involved turn white due to diminished blood supply. The digit(s) then turn blue because of prolonged lack of oxygen. Finally, the blood vessels reopen, causing a local "flushing" phenomenon, which turns the digit(s) red
treatment - drugs that cause dilation, avoiding large changes in temperature |
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Term
| What are the similarities between cardiac muscle and skeletal muscle? |
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Definition
1. Cardiac Muscle cell is composed of sarcomeres delineated by Z disks
2. Sarcomeres made of thick myosin filaments and thin actin filaments (with tropomysoin and troponin)
3. Contraction occurs according to sliding filament model – cross-bridging between myosin and actin
4. T-tubules invaginate cells and carry APs to cell interior enabling Ca+2 release from SR (underdeveloped in cardiac muscle)
5. Have excitation-contraction coupling (AP causing tension) |
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Term
| What are the differences between cardiac and skeletal muscle? |
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Definition
1.Sarcoplasmic reticulum not as well developed (most of the Ca2+ comes from the ECF)
2. T- tubule system runs in both transverse and longitudinal directions
3. Cells function as a syncytium (one unit)
4. Cells joined at intercalated disks
5. Cells held together by desmosomes
6. Cells connected by gap junctions
7. Cells are branched to form a network
8. Muscle fibers are morphologically different in different areas of the heart (i.e. ventricle, Purkinje fiber, SA node, AV node) |
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Term
| What are the different types of cardiac action potentials? |
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Definition
Ventricular AP phases:
0 – Depolarization / upstroke (Na+)
1 – 1st piece of repolarization
2 – Plateau (L-type channels)
3 – Rest of repolarization
4 – Baseline resting potential
(250 msec)
Atrial AP phases:
Similar to ventricle but 2 not as stable (fewer Ca+2 channels)
(150 msec)
SA phases:
0 – Upstroke (Ca+2; T- type channels)
1 & 2 - Absent
3 – Repolarization
4 – Spontaneous depolarization / pacemaker potential
(inward Na+ current, If) (150 msec)
uses "funny" channel and the depol. is unstable |
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Term
| Explain the different phases of the ventricular action potential |
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Definition
0 – Depolarization / upstroke - a lot of Na+ enters the cell
1 – 1st piece of repolarization - Na+ entering but more K+ exiting
2 – Plateau (L-type channels) - Ca2+ enters the cell to counteract the exit of K+
3 – Rest of repolarization - K+ exit overcomes Ca2+ entrance
4 – Baseline resting potential (250 msec) - Ca2+ influx stops and K+ and Na+ contribute to RMP (mostly K+ - remember permeability) |
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Term
| What is the length/tension relationship in cardiac muscle? |
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Definition
Resting length / left ventricular end diastolic volume/ preload
Length of muscle fibers at end of diastole just before
contraction
left ventricular end diastolic volume is the amount of blood right before contraction |
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Term
| What is Starlings law of the heart |
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Definition
| Starlings Law of the Heart: The greater the end-diastolic volume (preload), the greater the ventricular pressure that can be developed |
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Term
| What is relationship between ventricular pressure during systole and end-diastolic volume? |
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Definition
Pressure increases as fiber length increases (actively)
Reflects increasing degrees of thick/thin filament overlap
Increased cross-bridge formation
Greater tension
Maximal filament overlap happens when pressure is maximal (average amount of EDV) |
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Term
| What is the relationship between ventricular pressure and ventricular volume during diastole? |
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Definition
No contractions are occurring but
As EDV increases- pressure increases passively
Increasing pressure reflects increasing tension of the muscle fibers as they are stretched to longer lengths |
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Term
| How do you change the strength of cardiac contraction? |
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Definition
1. Change end-diastolic volume
2. Change cytosolic [Ca2+]
Contractility: intrinsic ability of myocardial cells to develop force at a given muscle length - correlates directly with [Ca2+] internally
To change contractility:
Neurohumoral factors i.e. NE increases sarcolemma permeability to Ca+2
Increasing the frequency of contraction = treppe (NO tetanus) |
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Term
| How can cardiac output be positively affected? |
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Definition
| Stimulation of SNS, catecholamines (NE, EPI), cardiac glycosides (digoxin) |
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Term
| How can cardiac output be negatively affected? |
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Definition
| Stimulation of PNS mediated via muscarinic receptors (ACh) |
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Term
| Explain the refractory periods in cardiac muscle |
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Definition
absolute refractory period - very long, no AP can be generated and prevents tetanus from occuring
relative refractory period - stimulus has to be stronger than usual to generate an AP
effective refractory period - can get depol.but it will not lead to an AP
supranormal period - more excitable than normal |
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Term
| Compare the phases of the atrial, ventricular, and SA node action potentials |
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Definition
SA Node has an AP duration of 150 msec, the upstroke is caused by inward Ca2+ influx, lacks a plateau, the phase 4 depol is caused by inward Na+ current through the funny channels
Atrial has an AP duration of 150 mscec, upstroke caused by inward Na+ current, plateau caused by inward Ca2+ current through L-type channels, no phase 4 depol
Ventricle is the same as atrial except the AP duration is 250 msec |
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