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FPP > Smooth Muscle Physiology > Flashcards

Smooth Muscle Physiology Flashcards

1
Q

Where is smooth muscle located?

A

Walls of hollow organs, including blood vessels (except for capillaries).

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2
Q

What are the 8 smooth muscle-containing organs?

A

Blood vessels:
- controls diameter
- vascular resistance
- distribution of blood flow and blood pressure
- venous capacitance
- central venous pressure

Gastrointestinal tract:
- Controls mixing and propulsion of GI contents

Bladder (detrusor), ureters, urethra:
- Urine storage and micturition (urination)

Uterus (myometrium):
- Smooth muscle responsible for labour

Respiratory system:
- Controls diameter of airways

Vas deferens and corpus cavernosum:
- Delivery of sperm for ejaculation

Fallopian tube:
- Mediates movement of eggs from ovaries to uterus

Iris and ciliary body:
- Control pupil diameter and focussing of the lens

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3
Q

morphology of smooth muscle

A

not striates (smooth), worm-shaped

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4
Q

regulation of smooth muscle

A
  • By the autonomic nervous system (ANS)
  • By hormones and locally released substances (autacoids)
  • In the GI tract, rhythmic contractions are initiated by pacemaker cells
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5
Q

what is the function of smooth muscle in iris and ciliary body

A

controls pupil diameter and focussing of lens

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6
Q

what is the function of smooth muscle in fallopian tube

A

mediates movement of eggs from ovaries to uterus

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7
Q

what is the function of smooth muscle in Vas deferens and corpus cavernosum

A

controls erection and ejaculation

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8
Q

what is the function of smooth muscle in uterus (myometrium)

A

responsible for labour

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9
Q

what is the function of smooth muscle in Bladder (detrusor), ureters, urethra

A

controls urine storage and micturition

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10
Q

what is the function of smooth muscle in GI tract

A

controls mixing and propulsion of GI contents

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11
Q

what is the role of smooth muscle in respiratory sysyem

A

controls diameter of airways

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12
Q

what is the role of smooth muscle in blood vessels

A

controls diameter, vascular resistance, distribution of blood flow and blood pressure

in veins it also control venous capacitance and central venous pressure

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13
Q

what is venous capacitance?

A

how much blood in the venous system

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14
Q

describe a large artery

A

low reisistance

conducting vessels

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15
Q

describe an arteriole

A

main reisstance vessels

control regional blood flow

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16
Q

describe a capillary

A

no smooth muscle

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17
Q

describe a venule

A

capacitance vessels

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18
Q

describe a large vein

A

low resistance

high capacitance vessels

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19
Q

2 types of Innervation of smooth muscle by the ANS

A

Multi-unit

Unitary

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20
Q

what is multi unit innervation fo smooth muscle by the ANS

A

Every smooth muscle cell has its own synaptic input

Allows for finer control of each muscle cell tone

IE: Iris, ciliary body, piloerector muscles
some vascular smooth muscle

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21
Q

what is unitary innervation fo smooth muscle by the ANS

A

Unitary
Not all cells have synaptic input, excitation is spread through tissue by gap junctions

Allows for co-ordinated contraction of many cells

GI tract, genitourinary, airways,
most vascular smooth muscle

UNITARY HAS GAP JUNCTIONS MULTI UNIT DOES NOT

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22
Q

in the structure of a smooth muscle, there are no sarcomeres or striations, instead there are?

A

Instead there are dense bodies and dense bands

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23
Q

what are Dense bands

A

Dense bands are protein aggregates that run along the surface of the cell

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24
Q

what are dense bands connected by

A

These are connected by intermediate filaments (protein filaments)

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25
Q

what are dense bodies made out of

A

The dense bodies are made out of the same protein that makes up the Z band in the sarcomere - this is called alpha actinin

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26
Q

what do dense bodies/ bands anchor

A

actin filament

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27
Q

whats the ration of actin: myosin in smooth muscle compared to striated muscle

A

higher actin:mysoin ratio compares to striated muscles

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28
Q

What does the sarcoplasmic reticulum store?

A

It both stores and release Ca2+.

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29
Q

What happens in smooth muscle contraction?

A

During contraction the cross bridge cycle brings these dense bodies closer together and because they’re dispersed through the cytoplasm, it shortens the cell and the cell also becomes fatter.

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30
Q

How are smooth muscle cells connected to neighbouring cells?

A

Via gap junctions.

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31
Q

What are the pathways for SKELETAL muscle contraction in striated muscle and how are they regulated?

A
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32
Q

What are the pathways for CARDIAC muscle contraction in striated muscle and how are they regulated?

A
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33
Q

What 2 ways is the contraction of smooth muscle regulated?

A

Autacoids
ANS

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34
Q

what is an Autacoids

A

Autacoids (also called local hormones): physiologically active factors released by cells which typically act in an autocrine or paracrine manner

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35
Q

what is the ANS

A

ANS: autonomic nervous system – a branch of the nervous system that controls the activity of the heart, visceral organs, blood vessels and glands

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36
Q

the contraction of smooth muscles throughout the body
is generally regulated by what?

A

by the ANS, by locally released factors, and by hormones.

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37
Q

what is the main stimulus for contraction in smooth muscles?

A

the main stimulus for contraction is noradrenaline released by the sympathetic nervous system, but vascular smooth muscle is also regulated by autacoids released from the vascular endothelium or from the tissues around the blood vessel, and also by hormones such angiotensin II.

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38
Q

What is the resting membrane potential range in blood vessels and airways?

A

Between -50 to -70 mV.

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39
Q

smooth muscles generate oscillations in membrane potential, what are these called

A

slow waves

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40
Q

Which types of smooth muscle generate slow waves, and what is their purpose

A

GI tract and uterus

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41
Q

out of GI tract and uterus, wich one is generated spontaneously and which one is driven by pacemaker cells

A

spontaneously = uterus
driven by pacemaker cells = GI tract

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42
Q

AP upstroke is due to what in smooth muscles?

A

voltage gated ca2+ channels

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43
Q

repolarisation is due to what in smooth muscles?

A

K+ channels

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44
Q

What causes the action potential in skeletal muscle?

A

The end plate potential opens voltage-gated sodium channels, causing the upstroke of the action potential.

Repolarization occurs due to the opening of voltage-gated potassium channels.

45
Q

How is the cardiac ventricular muscle action potential generated and maintained?

A

Depolarization is caused by currents from neighboring cells via gap junctions.

Voltage-gated sodium channels cause the upstroke.

A plateau phase occurs due to voltage-gated calcium channels.

Repolarization happens through voltage-gated potassium channels.

46
Q

What is a slow wave in GI tract smooth muscle?

A

Slow, periodic depolarizations of the membrane potential.

They last several seconds (longer than action potentials).

Slow waves occur continuously and are modulated by chemical stimuli (e.g., parasympathetic stimulation).

47
Q

How do slow waves and action potentials contribute to contractions in the GI tract?

A

Both depolarizations (slow waves and action potentials) open voltage-gated calcium channels, leading to contractions.

Contractions cause peristalsis, which propels GI contents.

Larger depolarizations with action potentials cause stronger contractions due to more calcium influx.

48
Q

Describe the electrical activity in vascular smooth muscle.

A

Membrane potential is stable without a stimulus.

Sympathetic nerve stimulation releases noradrenaline, opening receptor-gated channels and depolarizing the membrane.

If depolarization is large, action potentials occur due to voltage-gated calcium channels.

Repolarization happens via potassium channels.

49
Q

compare the action potentials in vascular smooth muscle compared to skeletal and cardiac

A

Action potentials in vascular smooth muscle are less developed than in skeletal or cardiac muscle.

50
Q

What causes depolarization and hyperpolarization in vascular smooth muscle?

A

Depolarization: Caused by vasoconstricting autacoids.

Hyperpolarization: Caused by vasodilating autacoids, opening potassium channels.

51
Q

How does depolarization and hyperpolarization affect vascular smooth muscle contraction?

A

Depolarization: Causes contraction; the strength depends on the degree of depolarization.

Hyperpolarization: Causes relaxation of the artery

52
Q

How do graded depolarizations differ from action potentials in smooth muscle?

A

Graded depolarizations are not all-or-nothing like action potentials.

The amplitude of the change in
membrane potential depends on the strength of the stimulus.

53
Q

What is the role of calcium influx in vascular smooth muscle?

A

Increased Ca²⁺ influx: Leads to contraction.

Decreased Ca²⁺ influx: Leads to relaxation.

54
Q

What happens to membrane potential and contraction when a constrictor stimulus is applied?

A

Causes depolarization.
Leads to increased Ca²⁺ influx and stronger contraction.

55
Q

What is the effect of a dilator stimulus on vascular smooth muscle?

A

Causes hyperpolarization.
Leads to decreased Ca²⁺ influx and relaxation of the artery.

56
Q

How does electrical activity in vascular smooth muscle differ from nerves or skeletal muscles?

A

It is more variable and depends on the stimuli acting on the artery.

Unlike nerves or skeletal muscles, action potentials are not all-or-nothing and do not all look the same.

57
Q

What initiates contraction in skeletal and cardiac muscle?

A

Contraction is initiated by a transient rise in intracellular Ca²⁺ concentration.

This rise always requires the firing of an action potential.

58
Q

How is the force of contraction regulated in skeletal muscle?

A

By the frequency of firing of the motor neuron that innervates the muscle fiber.

59
Q

How is the force of contraction regulated in cardiac muscle?

A

By the neurotransmitter noradrenaline, which increases the opening of voltage-gated Ca²⁺ channels.

Increased Ca²⁺ influx and release lead to a stronger contraction.

Cell stretch also regulates contraction by increasing the overlap between actin and myosin filaments.

60
Q

How does Ca²⁺ trigger cross-bridge cycling in striated muscle?

A
  1. Action potential increases intracellular 2. Ca²⁺ concentration.
  2. Ca²⁺ binds to troponin C.
  3. Tropomyosin shifts, exposing the myosin binding site on actin.
  4. Cross-bridge cycling begins, leading to contraction.
61
Q

What role does troponin and tropomyosin play in muscle contraction?

A

Troponin C: Binds Ca²⁺ to initiate contraction.

Tropomyosin: Moves away from the myosin binding site on actin, allowing cross-bridge cycling.

62
Q

How does noradrenaline affect cardiac muscle contraction?

A

It increases the opening of voltage-gated Ca²⁺ channels, causing greater Ca²⁺ influx and release, which enhances contraction strength.

63
Q

What are the 3 main pathways regulating smooth muscle contraction?

A

Ca²⁺ influx
Ca²⁺ release
Ca²⁺ sensitization

64
Q

what happens in ca2+ influx in pathways regulating smooth muscle contraction?

A

Ca²⁺ influx: Via Voltage-Operated Ca²⁺ Entry (VOCE) and Receptor-Operated Ca²⁺ Entry (ROCE).

65
Q

what happens in ca2+ release in pathways regulating smooth muscle contraction?

A

Ca²⁺ release: From the sarcoplasmic reticulum.

66
Q

what happens in ca2+ sensitisation in pathways regulating smooth muscle contraction?

A

Ca²⁺ sensitization: Regulates contraction without requiring additional Ca²⁺, mediated by Rho-kinase.

67
Q

What 3 stimuli activate smooth muscle contraction pathways?

A

Intrinsic slow waves: Found in the uterus and bladder.

Stretch: Leads to membrane depolarization.

Agonists: Such as ANS signals, autocoids, and hormones in blood vessels, airways, GI tract, and uterus.

68
Q

What role do Voltage-Operated Ca²⁺ Entry (VOCE) and Receptor-Operated Ca²⁺ Entry (ROCE) play in smooth muscle contraction?

A

VOCE: Ca²⁺ entry triggered by membrane depolarization.

ROCE: Ca²⁺ entry triggered by receptor activation (e.g., by agonists).

69
Q

How is smooth muscle contraction regulated independently of Ca²⁺?

A

Through Ca²⁺ sensitization, which enhances contraction via the Rho-kinase pathway without additional increases in cytoplasmic Ca²⁺ levels.

70
Q

How do pacemaker cells contribute to smooth muscle contraction?

A

Pacemaker cells in the GI tract generate intrinsic slow waves, which cause membrane depolarization and initiate contraction.

71
Q

What is the role of the sarcoplasmic reticulum in smooth muscle contraction?

A

Releases stored Ca²⁺ in response to signals, contributing to increased cytoplasmic Ca²⁺ levels and contraction.

72
Q

compare cross bridge cycling speed in smooth muscle and striated muscle

A

Cross-bridge cycling is much slower in smooth muscle compared to striated muscle.

This leads to a much lower requirement for ATP.

Smooth muscle can remain contracted indefinitely and doesn’t fatigue.

73
Q

How does Ca²⁺ regulate smooth muscle contraction?

A

Ca²⁺ binds to calmodulin (4 binding sites).

The Ca²⁺-calmodulin complex activates myosin light chain kinase (MLCK).

MLCK phosphorylates myosin regulatory light chains, increasing ATPase activity.

This allows myosin to interact with actin, initiating cross-bridge cycling and contraction.

74
Q

what opposes the action of myosin light chain kinase

A

Opposing the action of myosin light chain kinase is myosin phosphatase, which dephosphorylates the regulatory light chains, and so tends to inhibit contraction.

75
Q

How is smooth muscle relaxation achieved?

A

When intracellular Ca²⁺ decreases:
Calmodulin binding sites are no longer fully occupied.

MLCK activity decreases.

Myosin phosphatase dephosphorylates myosin light chains.

Cross-bridge cycling diminishes, leading to relaxation.

76
Q

What is Ca²⁺ sensitization in smooth muscle?

A

Ca²⁺ sensitization occurs when Rho-kinase phosphorylates myosin phosphatase, inhibiting its activity.

This increases myosin light chain phosphorylation, enhancing contraction for a given level of Ca²⁺.

77
Q

What is Ca²⁺ desensitization in smooth muscle?

A

Ca²⁺ desensitization is caused by activation of myosin phosphatase - it is activated by NO via cGMP

Protein kinase G (PKG) phosphorylates myosin phosphatase, increasing its activity.

This reduces myosin light chain phosphorylation, decreasing cross-bridge cycling and promoting relaxation.

78
Q

How does smooth muscle cross-bridge cycling differ from striated muscle?

A

Smooth muscle contraction is regulated by Ca²⁺ binding to calmodulin, not troponin.

Cross-bridge cycling in smooth muscle is slower but more energy-efficient, allowing prolonged contraction without fatigue.

79
Q

What is the role of MLCK in smooth muscle contraction?

A

Myosin Light Chain Kinase (MLCK):
Activated by the Ca²⁺-calmodulin complex.
Phosphorylates myosin regulatory light chains, enabling cross-bridge cycling and contraction.

80
Q

What happens to smooth muscle contraction when intracellular Ca²⁺ levels decrease?

A

MLCK activity decreases.
Myosin phosphatase activity dominates, reducing myosin phosphorylation.
Cross-bridge cycling and contraction diminish, leading to relaxation.

81
Q

What determines vascular tone?

A

Vascular tone is determined by a balance between constricting and dilating influences.

82
Q

What are 3 examples of constricting influences

A

Sympathetic nerves: Release noradrenaline to promote contraction.

Blood-borne hormones: Include adrenaline and angiotensin II.

Pressure/stretch: Activates contraction directly.

83
Q

what are 3 examples of dilating influences

A

Dilating influences include NO (Nitric Oxide), local tissue metabolites, and local hormones (autocoids).

84
Q

How does NO (Nitric Oxide) influence vascular tone?

A

NO is a vasodilator.
It acts on the endothelium to inhibit contraction of the smooth muscle.

85
Q

give 3 examples of tissue metabolites and describe what role these local tissue metabolites play in vascular tone?

A

Tissue metabolites such as CO₂, H₂O₂, and K⁺ act directly on the smooth muscle to cause relaxation, reducing vascular tone.

86
Q

What is the primary mechanism of sympathetic nerve action on vascular tone?

A

Sympathetic nerves release noradrenaline, which acts on smooth muscle to cause vasoconstriction.

87
Q

What triggers vascular smooth muscle contraction?

A

Noradrenaline, angiotensin II, and other vasoconstrictors act on α₁-adrenergic receptors.

Stretch also activates stretch-activated channels (SACs).

88
Q

What are the key channels involved in vascular smooth muscle contraction?

A

Stretch-Activated Channels (SACs): Allow Na⁺ entry, leading to membrane depolarization.

Receptor-Gated Channels (RGCs): Allow Na⁺ and Ca²⁺ influx.

Voltage-Gated Ca²⁺ Channels (VGCCs): Open due to depolarization, allowing Ca²⁺ influx.

89
Q

How does the α₁-adrenergic receptor pathway lead to Ca²⁺ release?

A

Activation of α₁ receptors stimulates phospholipase C (PLC).

PLC converts PIP₂ into DAG and IP₃.

IP₃ triggers Ca²⁺ release from the sarcoplasmic reticulum.

90
Q

What is the role of DAG and IP₃ in vascular smooth muscle contraction?

A

IP₃: Releases Ca²⁺ from the sarcoplasmic reticulum.

DAG: Activates protein kinase C, contributing to contraction.

91
Q

How does membrane depolarization contribute to vascular smooth muscle contraction?

A

Depolarization opens voltage-gated Ca²⁺ channels (VGCCs), allowing Ca²⁺ influx, which triggers contraction.

92
Q

What are the key sources of Ca²⁺ for vascular smooth muscle contraction?

A

Extracellular Ca²⁺: Through VGCCs and RGCs.
Intracellular Ca²⁺ stores: Released from the sarcoplasmic reticulum via IP₃.

93
Q

What stimulates the production of nitric oxide (NO) in endothelial cells?

A

Flow, bradykinin, acetylcholine, histamine, and prostacyclin (PGI₂) stimulate endothelial cells to produce NO.

94
Q

What is the role of nitric oxide (NO) in vasorelaxation?

A

NO activates guanylate cyclase (GC) in vascular smooth muscle cells.

GC converts GTP to cGMP, which mediates vasorelaxation.

95
Q

How does cGMP cause vasorelaxation?

A
  1. cGMP activates protein kinase G (PKG).
  2. PKG:
    Activates K⁺ channels, causing membrane hyperpolarization.
    Enhances Ca²⁺ desensitization, reducing contractility.
    Increases Ca²⁺ reuptake by SERCA and extrusion by PMCA, lowering cytosolic Ca²⁺ levels.
96
Q

What is the role of SERCA and PMCA in smooth muscle relaxation?

A

SERCA: Pumps Ca²⁺ back into the sarcoplasmic reticulum.
PMCA: Removes Ca²⁺ from the cytosol into the extracellular space.
Both lower cytosolic Ca²⁺, promoting relaxation.

97
Q

How does membrane hyperpolarization contribute to vasorelaxation?

A

Hyperpolarization reduces the activity of voltage-gated Ca²⁺ channels (VGCCs), decreasing Ca²⁺ influx and smooth muscle contraction.

98
Q

What is the function of phosphodiesterase (PDE) in the cGMP pathway?

A

PDE breaks down cGMP into GMP, terminating the relaxation signal.

99
Q

What triggers cyclic AMP (cAMP)-mediated vasorelaxation?

A

Activation of β₂-adrenergic receptors by substances like adrenaline, adenosine, and prostacyclin.
Stimulation of adenylate cyclase (AC) to convert ATP into cAMP.

100
Q

What is the role of cAMP in vasorelaxation?

A

cAMP activates protein kinase A (PKA), which:
2. Opens K⁺ channels, causing membrane hyperpolarization.
2. Reduces voltage-gated Ca²⁺ channel (VGCC) activity, lowering Ca²⁺ influx.
3. Enhances Ca²⁺ reuptake by SERCA and extrusion by PMCA.

101
Q

How do K⁺ channels contribute to cAMP-mediated vasorelaxation?

A

Opening of K⁺ channels leads to membrane hyperpolarization, reducing VGCC activity and decreasing Ca²⁺ influx, thereby promoting relaxation.

102
Q

What is the role of SERCA and PMCA in cAMP-mediated vasorelaxation?

A

SERCA: Pumps Ca²⁺ back into the sarcoplasmic reticulum, lowering cytosolic Ca²⁺.
PMCA: Removes Ca²⁺ from the cytosol to the extracellular space.
Both actions reduce cytosolic Ca²⁺, aiding relaxation.

103
Q

What role do metabolites and lipids play in cAMP-mediated vasorelaxation?

A

Metabolites like CO₂/H⁺, H₂O₂, and K⁺, as well as lipids like epoxyeicosatrienoic acids (EETs), activate K⁺ channels, enhancing hyperpolarization and relaxation.

104
Q

How does phosphodiesterase (PDE) regulate cAMP signaling?

A

PDE breaks down cAMP into AMP, terminating its vasorelaxation effects.

105
Q

in what 3 ways is Ca²⁺ removed during cAMP-mediated vasorelaxation?

A

SERCA: Reuptakes Ca²⁺ into the sarcoplasmic reticulum.

PMCA: Exports Ca²⁺ to the extracellular space.

Na⁺/Ca²⁺ exchanger: Removes Ca²⁺ from the cytosol.

106
Q

What is the effect of cAMP on VGCCs?

A

cAMP reduces VGCC activity through membrane hyperpolarization, decreasing Ca²⁺ influx and promoting relaxation.

107
Q

How does adrenaline act on vascular smooth muscle (VSM) expressing different adrenergic receptors?

A

If VSM expresses α₁ receptors: Response is contraction.

If VSM expresses β₂ receptors: Response is relaxation.

108
Q

Why is the adrenal medulla considered unique in the sympathetic nervous system?

A

There is no post-synaptic neuron; instead, adrenaline serves as the signal mediator, delivering systemic effects via the bloodstream.

109
Q

What receptors does adrenaline target and what are its effects?

A

α₁-adrenergic receptors: Vasoconstriction.
β₂-adrenergic receptors: Vasodilation.

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