Lecture 13 Smooth And Cardiac Muscle Flashcards

1
Q

Smooth muscle

A

Types: visceral and multiunit
Lack visible cross striations
Spindle shaped cells w/single nucleus
Cells usually arranged in sheets within muscle
No z line present - dense bodies
Diff function to skeletal muscle
No troponin or tropomyosin blocking cross bridges - light chains of proteins are attached to head of myosin molecules near “neck” region

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2
Q

Organisation of thick and thin filaments in smooth muscle cell

A

3 types of filament

Thick myosin
Thin actin
Filaments of inbetween size - part of cytoskeletal framework supporting cell shape
Myosin can only interact with actin when it’s light chains are phosphorylated

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3
Q

Arrangement of filaments

A

Thick and thin filaments are at slight diagonal from side to side in SM cell

Form a diamond shaped lattice

Myosin molecules arranged in thick filaments so cross bridges are present along entire length

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4
Q

Initiation of contraction

A

Triggered by Ca2+ dependent phosphorylation of myosin

Ca2+ binds to calmodulin which activates a kinase enzyme

This phosphorylates myosin activating myosin ATPase and hence myosin can interact with actin
Myosin is dephosphorylated by myosin light chain phosphatase

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5
Q

Ca2+ initiates contraction

A

Ca2+ is released from SR ( not as much as in skeletal) enters cell through membrane channels (voltage/ligand gated)

No T tubule system in smooth SR

Ca2+ removal is slow so longer contraction

Graded response

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6
Q

Role of Ca2+ in skeletal Vs smooth muscle

A

Smooth
Muscle excitation
Rise in cytosolic Ca2+ (mostly from extracellular fluid)
Series of biochem events
Phosphorylation of myosin in thick filament
Binding of actin and myosin at cross bridges
Contraction

Skeletal
Muscle excitation
Rais in cytosolic Ca2+ (entirely from intracellular SR)
Physical repositioning of troponin and tropomyosin
Uncovering of cross bridge binding sites on actin thin filament
Binding of actin and myosin at cross bridges
Contraction

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7
Q

2 major types of smooth muscle

A

Multi unit:
Neurogenic
Made of multiple discrete units - function independently - no gap junctions
Units must be separately stimulated by nerves to contract

E.g. large arteries, large airways, iris of the eye and hair follicles

Single unit:
Myogenic (don’t need nerve stimulation)
Fibres excited and contract as single unit
Gap junctions present
Contraction - slow and energy efficient
Function in syncytium

Found in hollow viscera: GI tract, blood vessels, uterus

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8
Q

Single unit SM may be phasic or tonic

A

Phasic - contracts in bursts, triggered by AP that lead to inc cytosolic Ca2+

Tonic- often partially contracted at all times “tone” due to relatively low resting potential
Doesn’t show bursts of activity like phasic SM but varies in increments above or below usual tonic state

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9
Q

Factors influencing smooth muscle contractile activity

A

Spontaneous depolarisation of cells

Signalling molecules - NTs from autonomic neurons and hormones

Local changes in extracellular fluid (pH, O2, osmolarity, ions)

Stretch

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10
Q

Myogenic response to stretch

A

Vascular smooth muscle cells respond to stretch by contracting
Smooth muscle can continue to develop tension even when considerably stretched

Stress relaxation response

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11
Q

Cardiac muscle

A

Found in the walls of the heart

Similar striations to skeletal muscle
- fibres joined in branching network
- z lines present

Cells joined at intercalated discs

T-tubule system

Innervated by autonomic nervous system

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12
Q

Cardiac muscle resting potential

A

Resting membrane potential approx 90mV

AP generated intrinsically

Functions as one unit

Each AP triggers full contraction followed by relaxation (can’t grade force contraction like skeletal muscle)

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13
Q

Cardiac muscle action potential

A

Spontaneous rapid depolarisation of cells occurs
Plateau phase
Slow repolarisation
Rhythmic firing
SA (sinoatrial) and AV (atrioventricular) nodes
Firing rate controlled by sympathetic and parasympathetic nervous systems

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14
Q

Firing of pacemaker cells

A

Movement of Na+ K+ and Ca²+ via ion channels
At -60mV Na channels open and slow inward current
Slow depolarisation (prepotential) Ca²+ channels open - depolarization

K+ channels open - repolarisation then when closed followed by slow depolarization (prepotential)

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15
Q

Pacemaker activity

A

Intrinsic automaticity of SAN = 100-110bpm
Activity of SAN normally controls heart rate
Nervous and hormonal control of SAN/AVN
AVN capable of independent activity
Latent pacemaker located in the conduction system e.g. Purkinje fibres can take over if SAN and AVN fail

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16
Q

Long refractory period prevents tetanus of cardiac muscle

A

2nd AP can’t be triggered until excitable membranes have recovered from the first
250ms~ plateau phase
300ms contraction phase

No summation or tetani