Autonomic, Smooth, Skeletal Muscle Flashcards

1
Q

What are the two anatomical divisions of the nervous system? What are the divisions composed of?

A

Central Nervous system (CNS) and Peripheral Nervous System (PNS)
CNS- composed of brain and spinal cord
PNS- includes neurons outside CNS.

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2
Q

What are the divisions that stem from Peripheral Nervous System? How do these divisions compare?

A

PNS can be divided into Afferent and Efferent divisions.
Afferent- signal towards brain in CNS. receive info from sensory organ to transmit towards CNS (ex: sight from eyes, tell brain you saw a dog in movie)
Efferent- signals away from CNS. go from CNS to PNS (ex: brain tells you to lift water bottle )

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3
Q

What divisions can Efferent portion of PNS be divided into?

What can autonomic part of PNS divide into? provide an example of this.

A

Efferent part of PNS:
1. Somatic efferent- VOLUNTARY activity
ex: contraction of muscles
2. Autonomic nervous system- INVOLUNTARY activity (we cannot control this), to control/regulate everyday needs and requirement of body; without CONSCIOUS participation from brain
Autonomic part of efferent PNS divide into sympathetic (fight/flight response) like skeletal muscle or Parasympathetic- rest/digest; seen in smooth muscle

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4
Q

Describe the synaptic mechanism in somatic nervous system, including the neurotransmitter and receptor used.

A

neurons at preganglionic fiber will release neurotransmitter Acetylcholine to activate NICOTINIC receptors for skeletal muscle. (Ach connects CNS to effector organ)

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5
Q

Describe the synaptic mechanism in an autonomic nervous system, including the neurotransmitter and receptor used.

A

Autonomic nervous system has divisions:
Sympathetic Nervous System: start with cell nuclei at preganglionic fiber than reach synapse and post ganglion fiber to meet target organ
in sympathetic: preganglionic fiber will use Ach (using nicotinic receptors) to connect CNS to ganglia, and in postganglionic fiber, NOREPINEPHRINE is used to connect ganglia to effector organ for SKELETAL muscle, using ALPHA or BETA receptors.
Sympathetic: ACH in preganglionic (nicotinic receptors) connect CNS to ganglia and EPINEPHRINE connect ganglia to effector organ for SMOOTH and CARDIAC muscle and ADRENAL gland.
Parasympathetic Nervous System: start with cell nuclei axon goes through .
In parasympathetic: preganglionic fibers: ACH used connect CNS to ganglia using nicotinic receptors and post ganglionic fibers use ACH to connect ganglia to effector organ in SKELETAL muscle using muscarinic receptors.

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6
Q

differentiate between the preganglionic and postganglionic fibers.
How do these fibers differ in length for parasympathetic vs sympathetic nervous system?

A

Preganglionic- neuron fibers connect CNS to ganglia
Postganglionic- neuron fibers connect ganglia to effector organ.
In sympathetic- Short preganglionic fibers, long post-ganglionic fibers
In parasympathetic- long preganglionic fibers and short post-ganglionic fibers.

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7
Q

What makes sympathetic nervous system different in adrenal glands?

A

The sympathetic nervous system has NO postganglionic fiber for adrenal glands, and uses epinephrine.

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8
Q

What is the parasympathetic nervous system also known as?

What kinds of nerves are part of the parasympathetic nervous system and distinguish where these nerves synapse at?

A

Parasympathetic nervous system aka CRANIAL SACRAL Nervous system.
cell nuclei of parasympathetic come from brain stem (cranial) and in sacrum
Cranial nerves 3, 7, 9 and 10
and Sacral nerves, S2, S3, and S4.
Cranial nerve 3- OCULOMOTOR synapse to EYE and carries parasympathetic fibers for synapses at CILIARY ganglia
Cranial nerve 7- FACIAL nerve synapses with parasymp to synapse at PTERYGOPALATINE and SUBMANDIBULAR
Cranial nerve 9- GLOSSOPHARYNGEAL synapse at OTIC ganglia
Cranial nerve 10- LARGEST cranial nerve in body, many outputs to many organs like the lungs, heart, liver, pancreas, stomach, intestine.
Sacral nerves: S2 S3 and S4 will stimulate Genital nervous system like bladder.

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9
Q

List the general functions or characteristics of Autonomic Nervous System.

A

1) to preserve homeostasis (parasymapthetic) and provoke reactions to protect the individual (Sympathetic)
2) afferent impulses from the viscera elicit reflex responses which generally cannot be controlled voluntarily.
3) Many fibers of the ANS are always active maintaining a basal tone in most organs (ex: a certain level of constriction of blood vessel by the sympathetic NS. A certain level of parasympathetic tone in the G.I. Tract.
4) Sympathetic and Parasympathetic nervous systems are generally antagonistic (ex: G.I. Tract, glucose control), but there are exceptions (ex: salivary glands, where both para and sympathetic stimulate secretion).
5) Activation of sympathetic nervous system is generally associated with defense mechanisms involving expenditure of energy, glycogenolysis, increased muscle tone, etc.
6) Activation of parasympathetic system- associated with conservative and restorative processes; decrease in blood pressure and body temperature.

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10
Q

Describe the motor efferents of parasympathetic Nervous system, including where these nerves are located.

A

The cranio-sacral motor division: the cells of origin for preganglionic fibers are located at 3 levels in CNS midbrain, medulla and sacral spinal cord.
Midbrain: Cranial nerve 3; from the Edinger-Westphal nucleus, preganglionic fibers go to the ciliary ganglion from where short postganglionic fibers go to terminate in the pupil and ciliary muscle.
Medulla or Bulbar outflow: Through facial, glossopharyngeal and vagus (7, 9, 10 cranial nerves)
-facial nerve: from superior salivary nucleus, preganglionic fibers going wit facial nerve go either to submandibular ganglion and via postganglionic fibers to innervate submaxillary and submandibular glands., or Pterygopalatine ganglions (post) which sends postganglionic fibers to lacrimal glands.
Glossopharyngeal nerve (9): from inferior salivary nucleus, preganglionic fibers go to otic ganglion and form here postganglionic fibers go to parotid gland
Vagus nerve- from the dorsal motor nucleus of vagus, preganglionic fibers go directly to thoracic and abdominal viscera. Postganglionic cells are located within the innervated organ.
The intermediolateral nuclei of S2-S4 sacral segments of spinal cord project to genitourinary organs and distal colon

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11
Q

Describe the different ways preganglionic fibers of Sympathetic system can pursue?

A

Cells of origin of preganglionic fibers are located in the lateral horns of the spinal cord (intermediolateral column) from 1st thoracic to the 2nd or 3rd lumbar segments.
A preganglionic fiber may pursue one of 3 courses after entering the ganglion through the ventral motor roots and white ramus:
A) can go to ganglion in the PARAVERTEBRAL sympathetic ganglionic chain at the SAME level of the chain, or go caudally or rostrally (can go down a level or up at higher position in chain) in the sympathetic chain before synapsing with a ganglionic cell.
B) Can BYPASS a paravertebral ganglion and synapse with a ganglionic neuron cell at an outlying sympathetic ganglion (PREVERTEBRAL or terminal ganglion).
C) Can directly innervate SECRETORY cells of the ADRENAL MEDULLA. The secretory cells (chromaffin cells) can secrete norepinephrine and epinephrine on sympathetic stimulation.
after synapse, post ganglion fiber go to target fiber (for prevertebral)

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12
Q

what are the 3 prevertebral ganglia for sympathetic nervous system?

A

Celiac, superior mesentery and and inferior mesentary

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13
Q

Describe the chemical transmission of nerve impulses and how a neuron is useful

A

Each neuron is a separate anatomic unit with no structural continuity between the units. Thus communication between the neurons is through release of chemical molecules called Neurotransmitters.

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14
Q

What are the two major Neurotransmitters in the Autonomic Nervous System and how do they aid in nerve transmission?

A

2 major neurotransmitters in ANS:

  1. Acetylcholine (ACh): ACh mediates all transmission of nerve impulses across autonomic ganglia in both sympathetic and parasympathetic nervous systems. Transmission from the autonomic postganglionic nerves to effector organs in parasympathetic system also involves release of ACh.
    2) Norepinephrine and Epinephrine: in the sympathetic mediates transmission nerve impulses from autonomic postganglionic nerves to effector organs.
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15
Q

Explain the whole process of cholinergic transmission.

A

Cholinergic transmission:
1. Synthesis of ACh: choline is transported from extracellular fluid into the cytoplasm of the cholinergic neuron by a carrier system that cotransports sodium and is inhibited by the drug, hemicholinum.
Choline reacts enzymatically with acetyl CoA to form acetylcholine
2. Storage of ACh: once synthesized, ACh is transported into synaptic vesicles where it is stored in granules
3. Release of ACh: when an action potential arrives at nerve ending, voltage-sensitive calcium channels in the presynaptic membrane open, causing an increase in concentration of intracellular calcium.
Elevated Ca+ promotes the fusion of synaptic vesicles within the cell membrane and release ACh into synapse.
4. Binding to receptor: ACh released from the synaptic vesicles bind to two different types of receptors: Nicotinic receptors or Muscarinic receptors.
Nicotinic receptors are found in all autonomic ganglia. Muscarinic receptors are found in cells of EFFECTOR organs.
5. Degradation of ACh: ACh is rapidly cleaved by acetylcholinesterase into choline and acetate.
6. Recycling of Choline: Choline may be recaptured by a high affinity transport system that pulls the molecule back into the neuron.

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16
Q

Discuss what occurs during the synthesis and release of Acetylcholine from parasympathetic nerve ending.

A
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17
Q

Discuss what occurs during the synthesis and release of norepinephrine from storage vesicles in SYMPATHETIC nerve endings

A

Synthesis and release of NE from vesicles in Sympathetic:

  1. Tyrosine is transported into the cytoplasm of the adrenergic neuron (Beta?), where the amino acid is hydroxylated to Dopa, by tyrosine-hydroxylase.
  2. Dopa is decarboxylated to form Dopamine
  3. once formed, Dopamine is transported into synaptic vesicles using an amine transporter.
  4. Dopamine is then hydroxylated to form Norepinephrine
  5. In adrenal medulla NE is methylated to form Epinephrine
  6. When an action potential arrives at the nerve terminal, this triggers an influx of Calcium ions from the extracellular fluid into the cytoplasm of the neuron. This causes the synaptic vesicles to release their contents into the synapse
  7. NE in the synapse is active for only a few msec. Ne binds to different adrenergic membrane receptors. its action is terminated by rapid reuptake, oxidation and by an enzyme: catechol-o-methyl transferase (COMT) present in the presynaptic membrane.
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18
Q

Explain how secondary messenger systems work

A

Secondary messenger molecules are produced in response to neurotransmitter binding to receptor, and translate the extracellular signal into response within the cell.

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19
Q

What is a neurotransmitter?

A

A neurotransmitter can be thought of a signal, and a receptor as a signal detector and transducer.

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20
Q

What are the two types of Cholinoreceptors in ANS? What are the two types of adrenergic receptors, and how do these receptors dffer when bound to neurotransmitters?

A

2 types of Cholinoreceptors in ANS:
NICOTINIC and MUSCARINIC
2 major adrenergic receptors:
1. Alpha (alpha 1 and alpha 2)
2. Beta (beta 1 and beta 2)
The receptors when bound to neurotransmitter activate different intracellular cell signals:
1. Direct regulation of ionic permeability: Nicotinic receptors are linked to membrane ion channels and directly alters ion permeability.
2. Regulation involving 2nd messenger molecules: the coupling of the muscarinic or adrenergic receptors to specific G-protein produces specific intracellular signals which in turn produces their specific effects on different organs.

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21
Q

What class of compounds does Epinephrine belong to?

A

Epinephrine belongs to a class of compounds known as catecholamines.

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22
Q

Describe the structural differences between smooth and skeletal muscle fibers and indicate the
structural similarities with respect to contractile units.

A

a

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23
Q

Describe the distinguishing characteristics of multi-unit and single-unit smooth muscles.

A

a

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24
Q

What are the functional uses of hypothalamic and brain stem centers?

A

Centers in various parts of the brain coordinate autonomic regulation of organ systems functions.
These systems include: Temperature regulation, thirst food intake, micturition (urination) , breathing and cardiovascular function.

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25
Q

What is the purpose of sensory neurons? Are they considered to be part of the Autonomic Nervous System?

A

Sensory neurons that are innervating involuntary organs are NOT considered part of ANS, but sensory input is important for autonomic function.
Ex:
1. sensory information concerning blood oxygen or CO2 levels is sensed by carotid bodies and is transmitted via cranial nerve 9
2. Baroreceptors in carotid sinus can send information to tractus solitaries in vasomotor center in medulla, which can then coordinate autonomic blood pressure regulation
3. Sensory innervation to visceral organs, blood vessels and skin forms afferent limb of autonomic reflexes.

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26
Q

*Diagram the intracellular pathways that control contraction and relaxation in smooth muscle

A

ass

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27
Q

*Explain how smooth muscle can develop and maintain force with a much lower rate of ATP
hydrolysis than skeletal muscle

A

ass

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28
Q

*Describe the mechanisms by which the smooth muscle cell can increase and decrease
intracellular calcium concentration

A

ass

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29
Q

*Describe the distinguishing characteristics of multi-unit and single-unit smooth muscles.

A

ass

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30
Q

*Describe the structural differences between smooth and skeletal muscle fibers and indicate the
structural similarities with respect to contractile units.

A

ass

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31
Q

*Draw and label a skeletal muscle at all anatomical levels, from the whole muscle to the
molecular components of the sarcomere. At the sarcomere level, include two different stages
of myofilament overlap

A

ass

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32
Q

*List the steps in excitation-contraction coupling in skeletal muscle, and describe the roles
of the sarcolemma, transverse tubules, sarcoplasmic reticulum, dihydropyridine receptors,
ryanodine receptors, and Ca2

A

Excitation-contraction coupling:

  1. ACH released from axon terminal binds to ACh receptor on the sarcolemma
  2. An action potential is then generated and travels down the T-tubule
  3. The spread of AP down T-tubules activates DHPR (dihydropyridine) receptors.
  4. DHPR (voltage SENSOR) sense change in membrane potential and changes its position (twists sideways) to become closer to RyR receptor.
  5. RYR receptor (ryanodine receptor) is now in close contact with DHPR and allows for Sarcoplasmic reticulum to release calcium (previously stored) in to cell due to change in voltage
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33
Q

*Describe the roles of ATP in skeletal muscle contraction and relaxation

A

ass

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34
Q

*Distinguish between an endplate potential and an action potential in skeletal muscle.

A

ass

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35
Q

*Compare a neuromuscular junction and chemical synapse between two neurons.

A

Similarities between Synapse and NMJ:
- 2 excitable cells separated by narrow cleft that prevents direct transmission of electrical activity
-Axon terminals store NT that are released by Calcium induced Exocytosis of storage vesicles
-binding of NT with receptor that opens membrane channels, permitting ionic movements that cause Change in Membrane potential.
Resultant change in MP is GRADED Potential (short distance signals)
Differences:
Synapse is a junction between TWO NEURONS
NMJ exists between a MOTOR neuron and a skeletal MUSCLE fiber.
- Synapse are always Excitatory (EPP) end plate potential
-NMJ are EXCITATORY (EPSP) post synaptic potential, or INHBITORY (IPSP)

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36
Q

*List some possible agents that affect neuromuscular transmission in skeletal muscle and the
mechanisms of action.

A
  1. Alters release of ACh:
    - Black widow spider venom- Explosive release of Ach; toxin can form pores in presynaptic membrane (excessive muscle contraction will occur, but NOT relaxation)
    - Clostridium botulinum toxin- blocks release of ACh: prevents contraction. This is used as a medicine (BOTOX) to treat chronic back pain due to muscle spasms.
  2. Blocks ACh Receptor:
    -Curare - reversibly binds to ACh receptor (NO contraction occurs). Derivatives of curare used to relax skeletal muscles during surgery.
    -Myasthemia Gravis-
    autoimmune condition in which antibodies inactivate ACh receptor (antibodies destroy communication between nerve and muscle).
    -Drug called NEOSTIGmine - short term Anti ACHase (prevents the enzyme from breaking down ACh into choline and acetic acid), increase likelihood of contraction (more ACh available)
  3. Prevents Inactivation of ACh:
    - Organophosphates (certain pesticides and nerve gases) - irreversibly inhibits AChase (causes contraction ) as Diaphragm unable to repolarize.
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37
Q

*Distinguish between an isometric and isotonic contraction

A

ass

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38
Q

*Distinguish between a twitch and tetanus in skeletal muscle and explain why a twitch is
smaller in amplitude than tetanus

A

ass

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39
Q

*List the energy sources of muscle contraction and rank the sources with respect to their
relative speed and capacity to supply ATP for contraction.

A

ass

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40
Q

*Compare the structural, enzymatic, and functional features of the 3 major fiber types of
skeletal muscle

A

ass

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41
Q

*Define a motor unit and describe the order of recruitment of motor units during skeletal
muscle contraction of varying strengths

A

ass

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42
Q

*Discuss the two major ways to increase whole muscle force development. Provide examples

A

ass

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43
Q

*Describe potential mechanisms that may contribute to sarcopenia.

A

ass

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44
Q

*What is the neurotransmitter and receptor for postganglionic fibers vs preganglionic fibers in sympathetic and parasympathetic? Which receptor is used for all ganglia in parasympathetic and sympathetic in ANS?

A

Postganglionic fibers:
neurotransmitter- Norepinephrine for sympathetic
receptor: alpha, beta receptors (adrenergic)
Preganglionic fibers of autonomic NS:
release neurotransmitter ACh for both sympathetic and parasympathetic.
Receptor for postganglionic parasympathetic- muscuranic
ALL ganglia on autonomic NS (both sympathetic and parasympathetic) use Nicotinic receptors
Epinephrine is not used for sympathetic (it is for smooth, cardiac muscle, gland, w/o postganglionic fiber)

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45
Q

*What happens to pupils if you overdose on Heroin? Overdose on Cocaine?

A

if you overdose on Heroin- pupils will constrict
overdose on Cocaine: pupils will DILATE, as cocaine will stimulate alpha receptor and affect peripheral nervous system . There will be less uptake of norepinephrine.

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46
Q

*What happens when there is too much ACh being released? What enzyme can help with this issue?

A

When there is too much ACh, causing constant release of it into synapse; there will be medical issues.
enzyme Acetylcholinesterase will break ACh down into Choline and Acetate.

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47
Q

*What is the one exception for what receptor is used and neurotransmitter released in sweat glands?

A

Exception:
Sweat glands have sympathetic control; receptor: muscarinic and neurotransmitter released is Acetylcholine (NOT norepinephrine)

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48
Q

Compare and contrast what happens in sympathetic vs parasympathetic for Pupils. Male genitalia? Bladder?

A
EYE: 
Sympathetic: pupils DILATE
Parasympathetic: pupils constrict
Male genitalia: 
sympathetic- controls EJACULATION
parasympathetic- controls erection
Bladder:
sympathetic: relax wall of bladder, prevent you from urinating
parasympathetic- relaxation of sphincter, CONTRACT bladder (allow you to pee)
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49
Q

Compare and contrast what happens in sympathetic vs parasympathetic for Heart, Vascular smooth muscle, bronicholes/lungs, and Liver.

A
  1. Heart:
    sympathetic- stimulate heart, increase heart rate (B1 receptor)
    parasympathetic- Decrease heart rate (M receptor)
  2. Vascular smooth muscle (blood vessels) are SYMPATHETIC for skin and skeletal muscle
    Skin (splanchnic)- Constricts (alpha 1 receptor)
    Skeletal muscle- DILATES (B2 receptor)
    Skeletal muscle- constrict (Alpha 1 receptor)
    Endothelium controlled by PARASYMPTHETIC:
    releases EDRF (endocyte releasing factor) using M receptor.
  3. Bronchioles:
    sympathetic - DILATES (B2 receptor)
    parasympathetic- constrict (M receptor)
  4. Liver: controlled by SYMPATHETIC; stimulate gluconeogenesis, glycogenolysis (alpha, B2 receptor)
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50
Q

What receptors are used for sympathetic functions vs parasympathetic functions? What is the exception?

A

Sympathetic mostly uses alpha and beta receptors
Parasympathetic mostly uses Muscarinic receptors.
Exception: Sweat glands are controlled by sympathetic and use Muscarinic receptors.

51
Q

what is the purpose phenylephrine?

A

This is a nasal decongestion that constricts blood vessel and reduces nasal mucosa.

52
Q

How do drugs affect ANS? What the the agonist and antagonist for the different receptors?

A

Drugs mimic the action of norepinephrine and epinephrine and also block sympathetic and parasympathetic at a level of receptor.
ex: Adreonreceptors: alpha 1: the agonists are NE, Phenylephrine and clonidine, the antagonists are phenoxybenzamine, prazosin
Beta 1 receptor: agonists are NE, Isoproterenol, antagonist are propanolol and metoprolol (important for heart disease)
Beta 2 receptor: agonist Epinephrine, Isoproterenol, albuterol, Antagonist: propranolol, butoxamine
Cholinoreceptors:
Nicotinic: agonists are ACh, Nicotine, and Carbachol (lowers pressure in eye); antagonists are Curare (relax skeleal muscle), Atropine, hexamethonium (blocks ganglionic receptor, but not NMJ)
Muscarinic: agonists are ACh, Muscarine and Carbachol, antagonist is Atropine (dilate pupil)

53
Q

What role does muscle play in the body? What is the function of muscle?

A

Muscle cells: CONTRACTION specialists in the body

they have highly developed ability to contract, develop tension and do work.

54
Q

What does contraction of muscle allow?

A

Contraction of muscle allows:
1. purposeful movement of the body in relation to the environment (ex: waving, stand on hand) skeletal
2. manipulation of external objects (ex: peeling fruit, move furniture); skeletal
3. propulsion of contents through hollow organs (contraction of smooth muscle,)
4. empty contents of organs to the environment (smooth muscle)
cardiac muscle only found in walls of heart (propel blood)

55
Q

What comprises the largest group of tissues in the body? How much of the body weight does it make up?

A

Muscle -larges group of tissues in body

makes up 1/2 of the body weight.

56
Q

what are the three types of muscle in the body. Describe their composition in the body, and in men vs women.

A
Three types of muscle: skeletal, smooth and cardiac
Skeletal muscle: 660 in adult human
-40% body weight in men
-32% body weight in women
Smooth and heart (cardiac) muscle = 10%.
57
Q

Describe what the classification of muscles are based on.

Include which muscles are striated, not striated, voluntary and involuntary.

A

Classification of muscles are based on appearance or our control of muscle (functional vs structural)
Skeletal and cardiac muscle: STRIATED
Smooth muscle- not striated
Skeletal muscle- VOLUNTARY (innervated by somatic NS)
smooth and cardiac muscle- INVOLUNTARY (innervated by ANS)

58
Q

Elaborate on the Organization of the Nervous system (CNS vs PNS)

A

Two main systems:
1. CNS- brain and spinal cord (central nervous system)
2. PNS- peripheral nervous system
In CNS:
1. Afferent division- sensory stimuli and visceral stimuli (input to CNS from periphery)
2. Efferent division- somatic nervous system, autonomic nervous system (output from CNS to periphery)
somatic nervous system- motor neurons for voluntary control (innervate skeletal muscle)
Autonomic nervous system- sympathetic Nervous system and parasympathetic nervous system (innervate smooth and cardiac muscle)

59
Q

Describe the levels of organization in a muscle (organ, muscle fiber, etc)

A

Whole muscle= organ
Muscle fiber= a cell
-relatively large (2.5 feet)
multinucleated (maintain protein production of large cell)
-Myofibril- intracellular structure (inside muscle fiber; organelle)
muscle, fascicle, fiber, myofibril (largest to smallest)
Thick and thin filaments of myofibril= myofilaments
myosin and actin- contractile proteins.
1 muscle fiber= 1 muscle cell.

60
Q

What is a sarcomere, and what is it’s role?

A

Sarcomere- smallest, functional unit on muscle. used for contraction of muscles.
Can be describes as 1 z line to the next z line, or 1 whole A band and 1/2 of each I band located on either side.

61
Q

What are the contractile proteins in muscle? Describe their characteristics.

A

Contractile proteins:
1. Thick filaments- contain several hundred myosin (heads and tails)
1 myosin molecule has 2 heads and tail (look like 2 golf clubs, 2 myosin subunits)
Heads- have actin binding site and Myosin ATPASE site. The heads are aka CROSS BRIDGES
2. Thin filaments - mostly ACTIN (form helix)
actin as a monomer from g actin or globular actin.
Each actin monomer has binding site for attachment with myosin cross bridge
actin monomers then form actin helix

62
Q

What are the regulatory proteins in muscle? Describe their characteristics.

A

Regulatory proteins: that make up thin filament
1. Tropomyosin- thread like (rope) structure that lays on actin to cover binding site for myosin to attach.
2.Troponin- 3 spherical subunits that stabilize sarcomere (place where Calcium binds to in muscle contraction)
The thin filament is made up of actin, tropomyosin and troponin.
These regulatory proteins (t-myosin and troponin) regulate how contraction occurs.

63
Q

What are the different changes that occur in banding pattern on muscle during shortening of sarcomere (muscle contraction)?

A

During muscle contraction:

  • A band stays SAME width
  • I band gets SHORTER with contraction
  • Sarcomere becomes shorter (bewtween z line and zline)
  • H zone becomes SHORTER during contraction
64
Q

What are the different changes that occur in banding pattern on muscle during shortening of sarcomere (muscle contraction)?

A

During muscle contraction:

  • A band stays SAME width
  • I band gets SHORTER with contraction
  • Sarcomere becomes shorter (bewtween z line and zline)
  • H zone becomes SHORTER during contraction
65
Q

What are the different components of sarcomere.

What is the medical mnemonic for muscle sarcomere?

A

A band- where thick and thin filaments overlap (thick and thin only found in A band
I band- remaining portion of thin filaments that do NOT project into A band
H zone- lighter area in middle of A band, where thin filaments do not reach
Z line - middle of I band; sarcomere is z line to z line
M line- mid point of sarcomere (gray area in between A band)
Mnemonics:
muscle sarcomere:
DArk bands is the A band
LIght band is the I band
Muscle sarcomere bands:
Zee Intelligent Animal Has Muscle
from Z line inward,

66
Q

Describe all things that result in muscle relaxation

A

What results in muscle relaxation:

  1. reuptake of Calcium by the SR
  2. No More AP (action potential)
  3. Removal of ACh at the end plate by AChase
  4. Filaments sliding back to their resting position.
67
Q

What occurs as a result of excitation of muscles?

A

aaa

68
Q

Describe the Steric Block model in Excitation-Contraction coupling, and what occurs

A

The Steric Block Model:
Physical blocking model that contains 2 actin units, 3 units of troponin and tropomyosin (blocking binding site for myosin)
Troponin has 3 units: T (binds tropomyosin) C(binds calcium) I (inhibits contraction)
In this process: an increase in calcium [ ]causes Calcium binds to troponin (c unit), troponin will then change its shape(rolled down), troponin-tropomyosin complex is PHYSICALLY pulled aside, and actin’s binding sites are now uncovered, allowing myosin to bind to actin (start contracting)

69
Q

What occurs in the cross-bridge cycling process in excitation-contraction coupling?

A

Cross-bridge cycling process:
Before cross bridge ever links:
-ATP is hydrolyzed by myosin ATPase
-ADP and P remain attached to myosin
-Energy stored in cross bridge (cocked and ready to be fired)
Process:
1. Cross bridge is energized (through hydrolysis of ATP and binding of ADP and P to myosin)
2. Calcium presence will remove inhibitory influence (between cross-bridge and actin)
3. energized myosin cross-bridge head can bind to to actin and undergo power stroke. close contact between actin and myosin x-bridge “pulls the trigger” of power stroke (bending of cross-bridge at angle). ADP and P released during this time.
4. Detachment- binding of fresh ATP to cross-bridge head breaks linkage between actin and myosin (decrease affinity for actin). x-bridge still bent
5. Cycle begins all over again with ATP being hydrolyzed, causing conformational change of head.

70
Q

What occurs when muscles return back to resting state?

A

Return to resting state:

  1. Neural excitation stops (no more AP being sent)
  2. Previously released Acetylcholine is broken down by AChase (enzyme convert ACh to choline and acetate)
  3. Muscle excitation stops
  4. Dihydropyridine channels close; diffusion of Calcium out of SR stops
  5. SERCA pumps Calcium back
  6. Actin’s binding sites are covered; and actin slides back into relaxed position away from center of sarcomere
71
Q

Distinguish between what occurs in the excitation of muscle cell compared to relaxation.

A

Excitation-Contraction Coupling
Resting state: The muscle is relaxed b/c regulatory proteins troponin and tropomyosin are covering actin’s binding site. No attachment is possible between actin and myosin filaments. Calcium is also absent in sarcoplasm; SERCA (sarco ER) is actively pumping (ATP) Calcium into SR , sarcoplasmic reticulum(for storage).
Excitation of Muscle:
1. ACh released from synaptic cleft and binds to nicotinic/cholinogernic receptor,
2. This causes Cation channels to open and allow Na+ ions to move in and from EPP (end plate potential). EPP is similar, but larger than EPSP (excitatory post-synaptic potential)
EPP is a chemically induced change in electrical potential (ACh causes redistribution of ions, and depolarization)
3. Depolarization causes AP to be created and sent down T-tubule, allowing for release of Calcium from SR and leading to muscle contraction.

72
Q

What are the roles
of the sarcolemma, transverse tubules, sarcoplasmic reticulum, dihydropyridine receptors,
ryanodine receptors, and Ca2 in skeletal muscle contraction (result of excitation)?

A

Sarcolemma: PM of muscle cell; form barrier to separate compartments inside vs outside of cell
T-tubules (transverse)- run perpendicular to surface of myofibril
SR- sarcoplasmic reticulum- modified ER, consists of interconnecting tubules surrounding each myofibril like a mesh sleeve; also holds Calcium
DHPR and RYR are Calcium channels
DHPR (dihydropyridine) are usually Voltage gated Calcium sensors, but in skeletal muscle they function as voltage sensor, sense change in potential and shift its position and activate RYR function
RYR (ryanodine receptor)- allows for Calcium to be released by Sarcoplasmic reticulum into cell, due to change in voltage.
both SR and T-tubules are specialized membranes that take AP from surface to center of the cell.

73
Q

Which molecule is responsible for removing steric inhibition for act of contraction? responsible for detachment of Crossbridge?

A

calcium- remove steric inhibition

ATP- responsible for detachment

74
Q

What happens during Rigor mortis?

A

Rigor mortis- there is no binding of fresh ATP to cause detachment (x-bridge still attached to actin) and stiffening of contraction of muscles after death. NO ATP available

75
Q

What are the three types of energy systems in skeletal muscle? Describe Immediate pathway and its unique components.

A

3 energy systems: immediate, non-oxidative and oxidative
1. Immediate- energy immediately available to support muscle contraction:
using ATPase (ATP and H2O make ADP , pi),
Creatine Kinase, (creatine phosphate and ADP make ATP and Creatine), Myokinase (2 ADP make ATP and AMP)
-immediate energy- produces a lot of energy FAST and used up quickly.
The [CP] is 5-6x the [ATP] in resting muscle.

76
Q

Describe the non-oxidative pathway and its characteristics.

A

Non-oxidative- energy sources in muscle- breakdown of glucose and glycogen (anaerobic pathway; no O2). Process glycogenolysis and glycolysis- rapid, fewer steps than Oxidative phosphorylation, but less efficient (more fuel/ATP for ox); non-ox produces lactic acid (muscle pH decreases).
non-ox ideal for 1st minute of exercise

77
Q

Describe oxidative pathway and its components. How does ATP generated in glycolysis (non-ox) compare to energy in oxidative

A

Oxidative- energy sources for muscle; carbohydrates, fats and certain amino acids.
energy used by athletes who run long distance (>400)
-slow pathway; a lot of steps required (Krebs cycle, ETC)
-requires O2.
-HIGHLY efficient
with oxidative process: glucose- will make 36 ATP
using palmitate (fatty acid) will get 129 ATP
with glycolysis: use glucose make only 2 ATP

78
Q

What is creatine phosphate? where is it used? Wht happens if creatine phosphate is in blood?

A

Creatine phosphate- high energy phosphate that reacts with ADP to create more ATP.
uses creatine kinase for CP+ ADP to make ATP and Cr
-Creatine phosphate is used in brain, heart and skeletal muscle
-if CP is found in blood, it can cause heart attack, skeletal damage.

79
Q

what is the purpose of immediate and non-oxidative pathways? what is maximal power?

A

The purpose of these pathways are for initial bursts of energy and for MAXIMAL POWER
maximal power- energy per unit time.
immediate has highest max power (36)
Immediate and non-ox are activated rapidly, producing energy at high rate; Oxidative slow to activate; produce energy at low rate.

80
Q

How do the energy systems compare?

A

the energy systems for muscle work for different types of activities
Immediate energy- used for POWER; 0-3 sec like weight lifting, shot put
Non-oxidative energy- used for SPEED; 4-50 sec like 100 to 400 m run, glycolysis,
Oxidative- used for ENDURANCE ; > 2min like >1500 long distance run, use cytosol and mitochondria, slower rate, takes a while to start

81
Q

What are the three major types of skeletal muscle fiber and what are they based on?

A

3 types of muscle fiber: Slow twitch, Fast twitch a and Fast twitch x
based on:
-speed of contraction (MYOSIN ATPase activity)
-type of metabolic pathway-ATP (oxidative or glycolytic)

Slow twitch- slow oxidative, high oxidative capacity (most fuel), low glycolytic, slow speed, high fatigue resistance (not prone to get fatigue)
Fast twitch a- fast oxidative/glycolytic, high glyco and ox, high motor unit strength fast speed, moderate fatigue resistance Fast twitch x- fast glycolytic (highest), low oxidative, fast speed, low fatigue resistance

82
Q

Distinguish between the different types of skeletal muscle fibers during exercise What are the fiber type ratios in the different athletes?

A

Type I fibers- LOW intensity aerobic exercise, daily activities
Type II a (WONDER FIBERS)- more force, faster fatigue than type I fiber, short high-intensity endurance events (1600 m run)
Type IIx- seldom used for everyday activities, short explosive sprints (100 m)
arm and leg fiber type are similar in one person
-endurance athletes: type 1 fiber predominates
-Power athlete- type II fiber predominates

83
Q

What are the major Fiber Type Determinants?

A
  1. Genetics-
    -determine which alpha-motor neurons innervate fibers
    these fibers differentiate base on alpha-motor neuron
  2. Training; muscle fiber influenced little by training
    -it is possible to transition from FOG to FG (fast glycolytic, type IIx)
    -endurance training can increase oxidative capacity of all 3 fiber types.
  3. Aging- muscles lose type II motor units
84
Q

What is a motor unit? What happens when motor neuron is activated? How does this affect contractions?

A

Motor unit- 1 motor neuron and all the muscle fibers it innervates
when a motor neuron is activated, all of its fibers it supplies are stimulated to contract simultaneously.
For stronger and stronger contractions, more and more motor units are recruited.

85
Q

What is the purpose of muscle recruitment? compare and contrast recruitment in type I and Type II fibers.

A

Motor Unit Recruitment- method for altering force production (power)
-Less force production- recruit smaller motor units (type I)
-More force production- recruit LARGER motor units (type II)
-precise, delicate movements- use less fibers, small; hand: one motor unit may contain DOZENS of muscle fibers.
Powerful, coarse movements- legs: one motor unit has 1,500 to 2,000 muscle fibers, large increments of power.

86
Q

Explain the size principle of motor neuron recruitment? Which motor units are recruited first?

A

Size Principle: the CNS increases muscle force by activating additional motor units in order of their increasing size, recruit beginning with SMALLEST
recruitment order : type I , type IIa, type IIx
-start with smaller units, then recruit larger motor units

87
Q

Explain how there is an increased use of recruitment in strength training.

A

In strength training:
-neural adaptations must take place before changes in muscle size
Early gains in strength- due to neural factors (which optimize recruitment patterns); recruit neural motor neurons.
Later : increasing cross-sectional area (hypertrophy) becomes more important (increase size of muscle)

88
Q

How is muscle tone achieved? Why is this necessary? How do you sustain muscle tone?

A

At rest, skeletal muscle exhibits muscle tone
Tone= small amount of tension due to weak, involuntary contractions of its MUSCLE FIBERS.
Purpose of tone: keep muscles PRIMED and ready for action.
Skeletal muscles are kept firm without producing movement.
To sustain muscle tone, motor unit groups alternately contract and relax
-very important in maintaining posture (ex: sitting)

89
Q

How can a force exerted by a muscle vary?

A

The force exterted by the SAME muscle can vary depending on whether we pick up:

  • a piece paper
  • book
  • 50 1b. weight
90
Q

What are the two factors that determine gradation(varying strength )of a whole muscle tension?

A

2 factors that determine gradation of whole muscle tension:

  1. the number of muscle fibers contracting within a muscle
    - number of motor units recruited
    - size of motor unit
  2. The Tension developed by each contracting fiber
    - frequency of stimulation
    - length-tension relationship
91
Q

Elaborate more on how the frequency of stimulation affects contraction of muscles. What is twitch summation? What is Tetanus?

A

Tension for each contracting fiber based on:
1. Frequency of stimulation- repetitive stimulation leads to contractions of LONGER duration and GREATER tension
- 1 muscle contraction= 1 twitch
Twitch summation (repeated twitch contractions): if a fiber has stimulated a second time before it has relaxed, it leads to greater tension
Tetanus- fiber stimulated so rapidly leading to no relaxation (smooth sustained muscle contraction); MAX tension

92
Q

*How does length of muscle contraction affect tension of muscle? What is length-tension relationship? (needs to be edited)

A

Length of muscle BEFORE it contracts, affects the amount of TENSION the muscle can generate
Length-tension relationship: the relationship between initial length and tension explained by number of CROSS-BRIDGES that is formed during contraction.
-decrease number of actin sites exposed to cross-bridges; thick filaments forced vs Z lines (length 1.27)
-length of 3.00: actin sites and cross-bridges no longer match up
-length of 3.65: muscle stretched to 70% longer than initial length, no cross-bridge activity, no contraction

93
Q

what are other factors that affect tension developed by each contracting fiber?

A
  1. Extent of fatigue
    - duration of activity
    - amount of asynchronous recruitment of motor units
    - type of fiber (fatigue-resistant vs fatigue prone)
  2. Thickness of fiber
    - type of fiber (small diameter oxidative vs large diameter glycolytic)
    - pattern of neural activity (hypertrophy vs atrophy)
    - amount of testosterone
94
Q

What are the two main types of muscle contraction?

A
  1. Isometric (SAME LENGTH)
    - muscle produces force, but does not change length
    -joint angle does not change
    - myosin cross-bridges form and recycle, no sliding; static
    ex; wall sit, plank
  2. Isotonic (SAME TENSION)
    - muscle produces force and changes length
    -joint movement produced; dynamic
    ex: running, walking
95
Q

What are the isotonic subtypes of contraction?

A

Concentric contraction
-muscle SHORTENS while producing force
-most familiar type of contraction
-sarcomere shortens
ex: bicep curl
Eccentric contraction
-muscle LENGTHENS while producing force
-cross-bridges form but sarcomere lengthens
ex: lowering heavy weight, walking downhill, lowering barbell back to ground
-causes most damage (when you feel most soreness)

96
Q

What is sarcopenia?

A

Sarcopenia- loss/atrophy of muscle with advancing age

-starting in our late 30’s to early 40’s most people lose 1/4 lb of muscle every year.

97
Q

What is the absolute centerpiece for being healthy, vital, and independent?

A

MUSCLE

98
Q

What are consequences and implications of Sarcopenia,(losing muscle mass)?

A

Consequences/clinical implications

  1. decrease in strength and power
    - risk of falling and fractures
  2. Decrease BMR(basal metabolic rate)
    - impaired thermoregulation
    - slower recovery from injury and damage
  3. Increase Body fat
    - decreased insulin sensitivity/increased insulin resistance
  4. Decreased Bone density
    - risk for osteoporosis
  5. Decreased Physical activity and VO2 max
    - fatigability
    - loss of mobility
    - Loss of independence- reduced quality of life
99
Q

What factors lead to muscle growth, balance growth and lead to muscle loss?

A

Hormones, exercise: increase muscle growth
Protein- balance for muscle growth and loss
malnutrition, inactivity, illness/injury- lead to muscle loss.

100
Q

Describe the hormonal mechansim changes with age

A

With age, there is an INCREASE in catabolic signals and loss of anabolic signals
Catabolic:
IGF-1, INSULIN INHBIT degradation of muscle
Cortisol and Cytokines, Ubiquitin promote the degradation of muscle
Anabolic:
-GH (growth hormone), IGF-I and T, IL-15 PROMOTE synthesis of muscle proteins
Cortisol, myostatin inhibit synthesis.
with age, decrease muscle fiber number and muscle fiber area atrophy decreases (size of muscle fiber decreases, especially in “Type 2” fiber area).
-decreased motor units in EDL muscle (extends toes: 75% type 2 muscle)

101
Q

How does the muscle respond to injury? How is this affected as we age?

A

Muscles from old animals are more susceptible to injury
-injury : muscles in old animals display prolonged, possibly irreversible structural and functional deficits.
Injury may play a role in development of muscle atrophy and weakness that occurs with aging.

102
Q

compare and contrast the loss of muscle mass with elderly and young, based on level of inactivity.

A
  • Healthy elders, with 10 days of inactivity will lose (10%) more total lean leg mass (3x more muscle loss, 1/3 time), which is higher than Inactivity duration for healthy young individual who have 28 days of inactivity
  • Elderly in hospital, 3 days of inactivity will lose 10% total lean leg mass, which is equal to mass lost for healthy elders with 10 days of inactivity; lower mass loss for healthy with 28 days of inactivity.
103
Q

What are the major factors that occur during age-related changes in muscle?

A

With age, connective tissue INCREASES and muscle fibers decrease

  • muscles become stringier and more sinewy (long, lean, stronger)
  • by age 80, 50% of muscle mass is lost(sarcopenia)
  • decreased density of capillary
  • reduced stamina
  • increased recovery time
  • regular exercise reverses sarcopenia
104
Q

What are solutions to changes in muscle mass as we age?

A

Strength Training: protects young and old muscles from injury
Eat enough protein
-spread protein throughout the day
-Leucine: most powerful amino acid that stimulates protein synthesis
-high leucine foods: cheese, soybeans, beef, chicken, seafood

105
Q

Explain the age-related dose response regarding elderly and young people. What happens if we ingest less than moderate.

A

The Age-related dose response- describes how the amount of protein consumed determines the amount of muscle protein synthesis that occurs.
Young people- if they consume more than 25 g of protein they will have about 50 mg of Muscle protein synthesis (a little higher than elderly)
Elderly- if consume more than 25 g of protein, also have around 45 mg muscle protein.
However, if both elderly and young consume less than 15 g protein, young will still be able to have a higher muscle protein synthesis than elderly (10 mg).
Elderly have a harder time increasing muscle protein synthesis when consuming less than 15 mg.

106
Q

*Explain the synergistic effect of protein and Exercise in elderly and Young?

A

In both young and elderly there is a 50% increase in protein synthesis levels when you move from fasting to having a protein meal. There is a 100% increase when you move from having a protein meal to combine protein with exercise. Hence, you reach the max level of protein synthesis when both young and elderly combine protein meal with exercise.

107
Q

What is the most powerful amino acid that stimulates protein synthesis?

A

LEUCINE

108
Q

Where is smooth muscle located and describe the tone (affect on function)

A

Smooth muscle located:

  • walls of hollow organs (gallbladder, uterus, bladder)
  • Tubes- (GI tract, blood vessels)
  • All smooth muscle exhibits tone (basal tension)
  • contractions superimposed on tone, which maintains SHAPE and Pushes content along
  • easy to constrict and dilate.
109
Q

Explain the types of functions that Smooth muscle is involved in. Why is smooth muscle so slow in function? What is the LATCH STATE?

A

Smooth muscle has DIVERSE functions.
1. Contraction- SLOWER and LONGER contractions than skeletal muscle
-g-enerates comparable force (same) force as Skeletal using 300 x LESS ATP.
-Smooth muscle gives up speed for ability to adapt and adjust
- respond to VARIETY OF STIMULI’: nerves, hormones, stretch, etc
LATCH State- prolonged contraction WITHOUT ATP input.
smooth also be phasically active (relax, contract, relax contract in stomach, intestines)

110
Q

differentiate between the smooth muscle structure compared to skeletal muscle. What does smooth muscle lack vs have?

A
Smooth muscle lacks: 
-sarcomeres (NO STRIATIONS)
-TROPONIN
-T-Tubules
Smooth muscle has: 
-Dense bodies (analogous to Z lines) that anchors actin; held in place by intermediate filaments
-TROPOMYOSIN, but role is unclear
-CAVEOLAE- indentations in sarcolemma
-may act like T-tubules
-SR (sarcoplasmic reticulum), but not well developed (not a lot of calcium)
111
Q

Elaborate on the arrangement of actin and myosin in smooth muscle. What is the benefit of long filaments?

A

In smooth muscle:
actin and myosin:
-oriented diagonally
-Diamond shaped lattice (not parallel with long axis)
-sliding causes cell to shorten and expand
-long thin filaments allow a large range of shortening to fully expel bladder.

112
Q

compare and contrast the two types of smooth muscle.

A

single unit: found in walls of hollow organs (gallbladder, uterus): the smooth muscle is excited as a single unit, contract as a unit. innervated by autonomic nerve fiber; muscles contract synchronously coupled by gap junctions
Multi unit: found in lungs and large arteries
-muscles excited individually, contract individually.

113
Q

Explain the excitation and contraction that occurs in single unit smooth muscle, including its unique characteristics.

A

Single Unit Smooth muscle:

  • only a few muscle fibers innervated in each group
  • cells can also be stimulated hormonally and by stretch
  • impulse spreads through GAP JUNCTIONS
  • whole sheet contracts as a unit
  • structure of Neuromuscular synapse is different
  • neurons have multiple varicosities (swelling of axons)
  • NO complex structure at synapse (No MEP)
  • one smooth smooth muscle can get input from both PNS and SNS.
114
Q

Describe the kind of electrical activity in smooth muscle, and elaborate on the two different types of fluctuations in electrical activity.

A

-SPONTANEOUS electrical activity initiated by pacemaker cells
-spreads throughout muscle
2 types of fluctuations in electrical activity:
1. Slow wave Potentials- coordinate muscle contractions in the gut by controlling appearance of a second type of depolarization event (APs)
2. Action (SPIKE) Potentials only occur at crests of slow waves.

115
Q

Explain the characteristics for the electrical activity of Multi Unit smooth muscle and how it parallel to skeletal muscle.

A

Multi Unit smooth muscle:
- seen in Iris (eye), piloerectors (hair on skin), large blood vessels
- received fine innervation allowing for regulation of individual cells
-cells are NOT CONNECTED electrically; these cells are stimulated and contract INDIVIDUALLY (like SKELETAL muscle)
Also like skeletal muscle,
-smooth muscle acts independently from other smooth muscle cells.
-Few gap junctions
-usually activated neurally.

116
Q

Differentiate between the excitation-contraction coupling in smooth muscle, compared to skeletal muscle

A

Extraction-Contraction Coupling in smooth muscle
-RMP (Resting membrane potential) is LOW (-50 to -60 mV)
- 30 mV above K+ equilibrium
-Higher Na+ permeability
-1 Na+ : 100 K+ in skeletal muscle
1 Na+ : 5 K+ in smooth muscle
-LONG AP= 10-50 ms (vs 2-3 ms in skeletal)
-NO voltage gated Na+ channels at motor end plate
-VOLTAGE-gated Ca^2+ channels (DIHYDROPyridine).

117
Q

What are the three Dihydropyridine receptors in the types of muscle? What are their characteristic?

A

Dihydropyridine receptors:
Skeletal: Voltage sensor
Cardiac: Voltage -dependent Ca+ channel; only lets in a little Ca+ in
Smooth: voltage -dependent Ca+ channel: only lets in ENOUGH Ca+ for AP (contraction to occur)

118
Q

What triggers contraction in smooth muscle? How is this achieved?

A

Calcium TRIGGERS Contraction in smooth muscle

  • -role of calcium: the state of THICK filaments (not thin filaments) are AFFECTED by Calcium
  • Calcium comes from
  • mostly from OUTSIDE the cell
  • Depolarization leads to voltage-gated Calcium channels opening
  • NTs (neurotransmitters), Hormones, open Calcium channels.
  • little Calcium is released from SR.
119
Q

Describe the mechanism of contraction in smooth muscle. How often is myosin on in smooth vs skeletal muscle?

A

In smooth muscle contraction:
1. Extracellular Calcium enters via:
-Voltage-gated channel (aka L-type aka DHPR)
-Ligand-gated channel (hormones, nerves)
-Stretch-activated channel (stretch)
2. Chemical activation:
-Calcium binds to CALMODULIN leading to activation of MYOSIN light chain kinase (MLCK)
-MLCK PHOSPHORYLATES light chain of myosin
-When myosin is phosphorylated, X-BRIDGES can form or break repeatedly.
-in smooth muscle: myosin is OFF
skeletal muscle: myosin is ALWAYS ON

120
Q

Describe the mechanism of relaxation in smooth muscle?

A

Smooth muscle relaxation occurs:
1. due to removal of contractile stimulus:
-decrease the ed [Ca^2+]
2. Direct action of substance that inhibits contractile mechanism
[increase ed MYOSIN PHOSPHATASE activity)
-phosphatase remove phosphate from MLC, inhibit it.
ratio of MLCK and MP (phosphatase) is important.

121
Q

Describe the pharmacological relaxation that occurs in smooth muscle? What leads to this relaxation? What occurs when cAMP or cGMP is increased? What are some drugs used?

A

In smooth muscle relaxation:

  • L-type Calcium channel blocker:
  • prevents the influx of calcium ions into smooth muscle, and leads to relaxation.
  • increase in cAMP or cGMP leads to relaxation
  • cAMP stimulated by EPI, (Epinephrine via Beta-2 receptor ) inhibits MLCK.
  • Epinephrine is used in treatment of bronchospasm of asthma
  • cGMP (nitroglycerin) stimulates myosin phosphatase which removes phosphate group from MLC, inhibits contraction; leads to relaxation of muscle
  • NO stimulates cGMP
  • Nitroglycerin (converted to NO in body) relaxes coronary arteries
  • Sildenafil- cGMP phosphodiesterase: used for erectile dysfunction
122
Q

How is tonic contraction of smooth muscle achieved?

A

Vascular smooth muscle (aorta) can sustain blood pressure without expending a lot of ATP: by developing FORCE: so cross-bridges can remain attached and cycle slowly, consume less ATP (Latch state)

123
Q

Explain the mechanism of tonic contraction for Smooth muscle.

A

Mechanism:
myosin will be dephosphorylated while it is still attached to actin
-when dephosphorylated, ATPase activity decreases
and it will be more difficult to release myosin heads from actin
-slow cross-bridge cycling occur (with low ATP use)

124
Q

What are the 5 main characteristics of smooth muscle?

A

Smooth muscle:

  1. INVOLUNTARY non-striated muscle associated with blood vessels and visceral organs.
  2. Overlapping myofilaments
    - sliding filaments generate force
  3. Increased Intracellular Calcium regulates myosin
  4. Calcium increased through:
    - mechanically gated Calcium channels
    - Ligand-gated Calcium channels (ANS, hormones, paracrine)
    - Voltage-gated Calcium channels
    - capable of PHASIC contraction (rapid contraction and relaxation) and TONIC contraction (slow and sustained contraction)