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Powell - Muscle 2
Cardiac and Smooth Muscle

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What is the structure of smooth muscle?
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
Explain multiunit smooth muscle
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
Explain unitary smooth muscle
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
What are the three types of smooth muscle action potentials?
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
What is the sequence of excitation-contraction coupling in smooth muscle?
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
What is latch-bridge formation?
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
Compare phasic and tonic contraction
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)
What are the different ways to increase ICF levels of Ca2+ in smooth muscle?
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;

4. Leak channels
What are the different ways to decrease ICF levels of Ca2+ in smooth muscle?
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
What is Raynaud's phenomenon?
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
What are the similarities between cardiac muscle and skeletal muscle?
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)
What are the differences between cardiac and skeletal muscle?
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)
What are the different types of cardiac action potentials?
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
Explain the different phases of the ventricular action potential
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)
What is the length/tension relationship in cardiac muscle?
Resting length / left ventricular end diastolic volume/ preload

Length of muscle fibers at end of diastole just before

left ventricular end diastolic volume is the amount of blood right before contraction
What is Starlings law of the heart
Starlings Law of the Heart: The greater the end-diastolic volume (preload), the greater the ventricular pressure that can be developed
What is relationship between ventricular pressure during systole and end-diastolic volume?
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)
What is the relationship between ventricular pressure and ventricular volume during diastole?
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
How do you change the strength of cardiac contraction?
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)
How can cardiac output be positively affected?
Stimulation of SNS, catecholamines (NE, EPI), cardiac glycosides (digoxin)
How can cardiac output be negatively affected?
Stimulation of PNS mediated via muscarinic receptors (ACh)
Explain the refractory periods in cardiac muscle
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
Compare the phases of the atrial, ventricular, and SA node action potentials
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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