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ACVIM General Boards > Cell Physiology > Flashcards

Cell Physiology Flashcards

1
Q

Structure of phospholipid membrane

A

Glycerol backbone = hydrophilic

2 fatty acid tails = hydrophobic

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2
Q

Substances that are soluble across the lipid bilayer

A

Lipid-soluble substances (O2, CO2, steroid hormones)

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3
Q

Substances that are NOT soluble across the lipid bilayer

A

Water-soluble substances (H2O, Na, Cl, glucose)

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4
Q

Integral proteins

A

Anchored in the membrane via hydrophobic interactions

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5
Q

Peripheral proteins

A

NOT embedded within the membrane; NOT covalently bound to the membrane - instead interact loosely with electrostatic interactions

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6
Q

Tight junctions

A

aka zona occludens; attachments between cells

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7
Q

Two types of tight junctions

A
  1. tight (impermeable)

2. leaky (permeable)

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8
Q

Gap junctions

A

the attachments between cells that permit intercellular communication

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9
Q

Characteristics of simple diffusion

A
  1. only form of transport that is NOT carrier mediated
  2. downhill (down an electrochemical gradient)
  3. passive (does not require metabolic energy)
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10
Q

Diffusion equation

A

J = -PA(C1 - C2)

*the minus sign indicates the direction of flow is from high to low concentration

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11
Q

Permeability (P)

A

The ease with which a solute diffuses through a membrane; depends on characteristics of both the solute and the membrane

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12
Q

Factors that increase permeability

A
  1. increase oil/water partition coefficient of the solute–>increased solubility in the lipid membrane–>increased permeability
  2. decreased radius of the solute–>increases the diffusion coefficient and speed of diffusion
  3. decreased membrane thickness–>decreased diffusion distance
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13
Q

Features of solutes with the highest permeability in lipid membranes

A
  1. small

2. hydrophobic/lipophilic

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14
Q

Two types of carrier mediated transport

A
  1. facilitated diffusion

2. primary and secondary active transport

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15
Q

Facilitated diffusion

A

Diffusion down a gradient, just via a transporter

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16
Q

Three general characteristics of carrier-mediated transport

A
  1. stereospecificity
  2. saturation
  3. competition
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17
Q

Characteristics of facilitated diffusion

A
  1. downhill
  2. passive
  3. more rapid than simple diffusion
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18
Q

Example of facilitated diffusion

A

glucose transport in muscle and adipose tissue

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19
Q

Characteristics of primary active transpot

A
  1. uphill (against an electrochemical gradient)

2. requires direct input of metabolic energy in the form of ATP

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20
Q

Examples of primary active transport

A
  1. Na-K-ATPase (3Na/2K)–>provides energy in the terminal bond of ATP
  2. Ca2+-ATPase (Ca2+ pump)
  3. H-K-ATPase (proton pump
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21
Q

Specific inhibitors of Na-K-ATPase

A

Cardiac glycoside drugs:

  1. ouabain
  2. digitalis
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22
Q

Location of the calcium pump

A
  1. sarcoplasmic reticulum
  2. endoplasmic reticulum
  3. cell membranes
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23
Q

Location of the proton pump

A
  1. gastric parietal cells

2. renal alpha-intercalated cells

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24
Q

Characteristics of secondary active transport

A
  1. transport of 2 or more solutes is coupled
  2. one of the solutes (usually Na) is transported downhill to provide energy for the uphill transport of the other solute(s)
  3. metabolic energy is provided indirectly
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25
Q

Effect of inhibition of Na-K-ATPase on secondary active transport

A

it inhibits secondary active transport because you won’t get any energy produced from moving Na in that direction

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26
Q

Cotransport

A

= symport; solutes move in the SAME direction across the membrane

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27
Q

Examples of cotransport

A
  1. Na-glucose cotransport

2. Na-K-2Cl cotransport

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28
Q

Locations of Na-glucose cotransport

A
  1. small intestines

2. renal early proximal tubule

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29
Q

Locations of Na-K-2Cl cotransporter

A
  1. renal thick ascending limb
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30
Q

Countertransport

A

= exchange/antiport; solutes move in OPPOSITE directions across the cell membrane

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31
Q

Examples of countertransport

A
  1. Na-Ca2+ exchange

2. Na-H exchange

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32
Q

MOA of Na-glucose cotransport

A

glucose is transported uphill (into the cell); Na is transported down hill (into the cell) - energy comes from moving Na downhill
*NOTE: inhibition of the Na-K-ATPase will inhibit Na-glucose cotransport

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33
Q

MOA of the Na-Ca2+ cotransport /exchange

A

Ca moves uphill from low intracellular Ca to high extracellular Ca; Na and Ca move in opposite directions across the cell membrane; energy comes from moving Na downhill (into the cell)

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34
Q

Osmolarity

A

The concentration of osmotically active particles in a solution (Osm/L)

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35
Q

Osmolarity equation

A 
osmolarity = g x C
g = the number of particles in solution (Osm/mol)
C = concentration (mol/L)
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36
Q

Example of how to count the number of particles in solution (g)

A

NaCl = 2; glucose = 1

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37
Q

van’t Hoff’s law

A

= the equation used to calculate osmotic pressure; the osmotic pressure depends on the concentration of osmotically active particles
Equation = pi = g x C x RT
pi = osmotic pressure (mmHg or atm)
g = number of particles in solution (osm/mol)
C = concentration (mol/L)
R = gas constant (0.082 Latm/molK
T = absolute temperature (K)

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38
Q

Example of osmotic pressure increasing

A

Osmotic pressure increases as the solute concentration increases; a solution of 1 M CaCl2 has a HIGHER osmotic pressure than a solution of 1 M KCl because the number of osmotically active particles is HIGHER in the former

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39
Q

Colloid osmotic pressure

A

= oncotic pressure = the osmotic pressure created by proteins (e.g. plasma proteins)

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40
Q

Reflection coefficient

A

Epsilon; a number between zero and one that describes the ease with which a solute permeates a membrane

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41
Q

Reflection coefficient = 1

A

= the solute is impermeable
–>retained in the original solution–>creates an osmotic pressure–>causes water flow
Example: serum albumin

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42
Q

Reflection coefficient = 0

A

= the solute is completely permeable
–>will NOT exert an osmotic effect–>will NOT cause water flow
Example: urea = an ineffective osmole

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43
Q

Effective osmotic pressure

A

= the osmotic pressure calculated by van’t Hoff’s law multiplied by the reflection coefficient

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44
Q

Ion channels

A

Integral proteins that span the membrane and when open, permit the passage of certain ions

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45
Q

Features of ion channels

A
  1. selective (based on size of channel and distribution of charges that line it)
  2. may be open or closed
  3. conductance of the channel depends on the probability that the channel is open
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46
Q

Example of a ligand-gated channel

A

Nicotinic receptor for acetylcholine at the motor end plate; the ion channel opens when Ach binds to it–>permeable to Na and K–>motor endplate depolarizes

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47
Q

Diffusion potential

A

= the potential difference generated across a membrane because of a concentration difference of an ion

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48
Q

Features of diffusion potential

A
  1. size of diffusion potential - depends on the size of the concentration gradient
  2. sign of the diffusion potential - depends on whether the diffusing ion is positively or negatively charged
  3. created by diffusion of VERY FEW ions–>do NOT result in changes in concentration of the diffusing ions
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49
Q

Equilibrium potential

A

= the potential difference that would exactly balance (oppose) the tendency for diffusion down a concentration difference

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50
Q

Electrochemical equilibrium

A

= the chemical and electrical driving forces that act on an ion are equal and opposite = no further net diffusion of ions occurs

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51
Q

Nernst equation

A

= equation used to calculate the equilibrium potential at a given concentration difference of a permeable ion across a cell membrane; tells us at what potential would the ion be at electrochemical equilibrium

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52
Q

Intuitive approach to determine if the sign for the equilibrium potential is correct

A

intracellular Na = 15mM vs. extracellular Na = 150mM
The Na is HIGHER in the extracellular fluid than the intracellular fluid–>Na ions will diffuse from the extracellular to the intracellular space, making the INSIDE of the cell positive, so Ena = +65mV
movement into the cell = +

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53
Q

Approximate values for equilibrium potentials in nerve and skeletal muscle

A 
Ena = +65mV
Eca = +120mV
Ek = -85mV
Ecl = -85mV
*NOTE: the positive ions that have higher extracellular concentrations will have a POSITIVE equilibrium potential; the positive ions that have lower extracellular concentrations and will move OUT of the cell will have a negative
into cell positive ion = +
out of cell positive ion = -
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54
Q

Driving force on an ion

A

= the difference between the actual membrane potential (Em) and the ion’s equilibrium potential (calculated with the Nernst equation); i.e. the difference between the actual membrane potential and what the ion would “like” the membrane potential to be (= at its equilibrium potential)

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55
Q

Current flow

A

= occurs if there is a a driving force on the ion AND the membrane is permeable to that ion

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56
Q

Direction of flow

A

= same as the direction of the driving force

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57
Q

Factors determining the magnitude of current flow

A
  1. size of driving force

2. permeability of the ion

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58
Q

Resting membrane potential

A

= the measured potential difference across the cell membrane; expressed as the intracellular potential relative to the extracellular potential; example: the resting membrane potential of -70mV = 70mV with the cell NEGATIVE compared to the extracellular space

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59
Q

Ion with the highest permeability

A

= the ion whose equilibrium potential the membrane potential is closest to; example: the resting membrane potential of a nerve = -70mV, which is closer to the K+ equilibrium potential of -85 than Na of +65, therefore, at rest, the never membrane is MORE PERMEABLE to K+ than to Na+

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60
Q

Depolarization

A

= makes the membrane potential less negative (i.e. the inside of the cell becomes LESS NEGATIVE due to the influx of positive ions)

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61
Q

Hyperpolarization

A

= makes the membrane potential MORE NEGATIVE (the inside becomes more negative due to the efflux of positive ions)

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62
Q

Inward current

A

= the flow of positive charge into the cell–>depolarization of the cell membrane

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63
Q

Outward current

A

= the flow of positive charge out of the cell–>hyperpolarization of the cell membrane

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64
Q

Threshold

A

= the membrane potential at which the action potential is inevitable; where the net inward current becomes larger than the net outward current

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65
Q

Features of action potentials (3)

A
  1. stereotypical size and shape
  2. are propagating
  3. are all-or-none
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66
Q

Ionic basis of nerve action potentials

A

At rest, inactivation gates for Na are open (opened by repolarization of the membrane), but the activation gates are closed (only open at the time of depolarization)

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67
Q

Overshoot

A

= the brief portion of the peak of the action potential when the membrane potential becomes positive

68
Q

Depolarization–>

A
  1. Opening of the activation gate of Na channel
  2. Closing of the inactivation gate of the Na channel
  3. Slow opening of the K channel
69
Q

Undershoot

A

= hyperpolarization afterpotential; K+ conjudctance remains higher than at rest for some time after closure of the Na channels, during which the membrane potential is driven close to the K+ equilibrium potential

70
Q

Inhibitors of voltage-sensitive Na channels that ABOLISH action potentials

A
  1. tetrodotoxin (TTX)

2. lidocaine

71
Q

Inhibitors of voltage-gated K+ channels

A
  1. tetraethylammonium (TEA)
72
Q

Absolute refractory period

A

= the period during which anther action potential CANNOT be elicited, no matter how large the stimulus; REASON: the inactivation gates of the Na channels are closed when the membrane is depolarized and they remain closed until repolarization occurs

73
Q

Relative refractory period

A

= begins at the end of the absolute refractory period and continues until the membrane potential returns to the resting level; an action potential CAN be elicited only if a larger than usual inward current is provided; REASON: the K+ conductance is higher than at rest, therefore the membrane potential is closer to equilibrium (further from the threshold) = more inward current is required to bring the membrane to threshold

74
Q

Accommodation

A

= when the cell membrane is held at a depolarized level such that the threshold potential is passed without firing an action potential; occurs bc deplarization closes inactivation gates on the Na channels

75
Q

Result of hyperkalemia on muscles

A

hyperkalemia–>skeletal muscle membranes are depolarized by the high serum K+ concentration (since usually the inside of the cell has a higher K+ concentration); action potentials do NOT occur because the inactivation gates of Na channels are closed by depolarization–>muscle weakness with hyperkalemia

76
Q

MOA of propagation of action potentials

A

Spread of local currents to adjacent areas of membrane

77
Q

Factors that increase conduction velocity along a nerve

A
  1. increased fiber size

2. myelination

78
Q

Saltatory conduction

A

= the form of conduction in myelinated nerves in which action potentials occur only at the nodes of Ranvier (= the gaps in the myelin sheath)

79
Q

Two general types of neurotransmitters

A
  1. inhibitory neurotransmitters

2. excitatory neurotransmitters

80
Q

Inhibitory neurotransmitters–>

A

Hyperpolarization of the postsynaptic membrane

81
Q

Excitatory neurotransmitters–>

A

Depolarize the postsynaptic membrane

82
Q

General steps at neuromuscular synapses

A
  1. Depolarization of the presynaptic terminal
  2. Calcium enters the presynaptic terminal
  3. Release of neutrotransmitter into the synaptic cleft
  4. Neurotransmitter binds to postsynaptic membrane receptors–>
  5. Change in permeability to ions and the membrane potential
  6. Depolarization of adjacent membrane potential to threshold–>action potential
  7. Action potentials are then followed by contraction
83
Q

Neurotransmitter of the neuromuscular junction

A

Acetylcholine

84
Q

Postsynaptic membrane receptor of the neuromuscular junction

A

Nicotinic receptors = ligand-gated channel (ligand = ACh) = Na and K ion channels

85
Q

Choline acetyltransferase

A

= enzyme that catalyzes formation of Ach from acetyl coenzyme A (CoA) and choline in the presynaptic terminal

86
Q

Result of ACh binding to the nicotinic receptors

A

ACh binds to the alpha subunits of the nicotinic ACh receptor–>conformational change–>increases conductance to Na and K

87
Q

End plate potential (EPP) of the postsynaptic membrane

A

= a depolarization of the specialized muscle end plate; NOT an action potential; can result in depolarization of adjacent muscle membrane to threshold

88
Q

Miniature end plate potential

A

MEPP; the smallest EPP produced by the contents of one synaptic vesicle (one quantum)

89
Q

Acetylcholinesterase (AChE)

A

= enzyme on the muscle end palte that degrades ACh into acetyl CoA and choline; 50% of the choline is taken back into the synaptic ending via choline cotransporters and used to make new ACh

90
Q

Neostigmine

A

= acetylcholinesterase inhibitor; blocks degradation of ACh–>prolongs ACh’s action at the muscle end plate–>increases the size of EPP

91
Q

Hemicholinium

A

Blocks choline reuptake and depletes presynaptic endings of ACh stores

92
Q

Myasthenia gravis MOA

A

= antibodies to the ACh receptor

93
Q

Characteristics of myasthenia gravis

A
  1. skeletal muscle weakness and fatigue due to a reduced number of ACh nicotinic receptors on the muscle end plate
  2. reduced size of EPP–>more difficult to depolarize the membrane to threshold–>more difficult to produce an action potential
94
Q

Treatment of myasthenia gravis

A

Neostigmine

95
Q

Four main agents affecting neuromuscular transmission

A
  1. botulinum toxin
  2. curare
  3. neostigmine
  4. hemicholinium
    THINK in order of starting at the presynaptic terminal and going to the postsynaptic terminal
96
Q

MOA of botulinum toxin and effects on neuromuscular transmission

A 
MOA = blocks release of ACh from presypaptic terminals
Effect = total blockade
97
Q

MOA of curare and effects on neuromuscular transmission

A 
MOA = competes with ACh for receptors on motor end plate
Effect = decreases size of EPP; maximal dose produces paralysis of respiratory muscles and death
98
Q

MOA of neostigmine and effects on neuromuscular transmission

A 
MOA = inhibits acetylcholinesterase
Effect = prolongs and enhances action of ACh at the muscle end plate
99
Q

MOA of hemicholinium and effects on neuromuscular transmission

A 
MOA = blocks reuptake of choline into presynaptic terminal
Effect = depletes ACh stores from the presynaptic terminal
100
Q

Types of synaptic transmission

A
  1. one-to-one synapses

2. many-to-one synapses

101
Q

One-to-one synapses

A

= an action potential in the presynaptic elements (the motor nerve) produces an action potential in the postsynaptic element (the muscle)
Location = neuromuscular junction

102
Q

Many-to-one synapses

A

= an action potential in a single presynaptic cell is insufficient to produce an action potential in the postsynaptic cell and instead many cells synapse on the postsynaptic cell to depolarize it to threshold
Location = spinal motoneurons

103
Q

Excitatory postsynaptic potentials (EPSPs)

A

= inputs that depolarize the postsynaptic cell, bringing it closer to threshold and closer to firing an action potential; caused by opening of channels permeable to Na and K, similar to the ACh channels

104
Q

Excitatory neurotransmitters

A
  1. acetylcholine
  2. norepinephrine
  3. epinephrine
  4. dopamine
  5. glutamate
  6. serotonin
105
Q

Inhibitory postsynaptic potentials (IPSPs)

A

= inputs that hyperpolarize the postsynaptic cell, moving it away from threshold and farther from firing an action potential; caused by opening of Cl channels–>the membrane potential is hyperpolarized toward the Cl- equilibrium potential (-90mV)

106
Q

Inhibitory neurotransmitters

A
  1. GABA (gamma-aminobutyric acid)

2. glycine

107
Q

Spatial summation

A

= when 2 excitatory inputs arrive at a postsynaptic neuron simultaneously–>greater depolarization

108
Q

Temporal summation

A

= when 2 excitatory inputs arrive at a postsynaptic neuron in rapid succession–>add in a stepwise fashion

109
Q

Facilitation, augmentation, and postetanic potentiation

A

= occur after tetanic stimulation of the presynaptic neuron; depolarization of the postsynaptic neuron is GREATER than expected because greater than normal amts of neurotransmitter are released, possibly because of the accumulation of Ca2+ in the presynaptic terminal

110
Q

Norepinephrine

A

= the primary neurotransmitter released from postganglionic sympathetic neurons

111
Q

Norepinephrine
Area of synthesis
Postsynaptic membrane receptor
Removal form synapse

A

Area of synthesis = nerve terminals
Postsynaptic membrane receptor = alpha or beta receptors
Removal from synapse
1. reuptake
2. metabolized in presynaptic terminal by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT)

112
Q

Metabolites of norephinephrine metabolism by COMT and MAO

A
  1. doma
  2. normetanephrine
  3. MOPEG
  4. VMA (vanillymandelic acid)
113
Q

Enzyme synthesizing epinephrine

A

phenylethanolamine-N-methyltransferase - synthesizes epinephrine from norepinephrine by transferring a methyl group from S-adenosylmethionine

114
Q

Location of epinephrine synthesis

A

Adrenal medulla

115
Q

Dopamine
Location
Release
Metabolism

A

Location: midbrain neurons
Released from: hypothalamus
Metabolized by: MAO and COMT

116
Q

Dopamine receptors

A
  1. D1–>activates adenylate cyclase via a Gs protein

2. D2–>inhibit adenylate cyclase via a Gi protein

117
Q

Parkinson disease

A

degeneration of dopaminergic neurons that use the D2 receptors

118
Q

Schizophrenia

A

increased levels of D2 receptors

119
Q

Cascade to epinephrine formation

A
  1. tyrosine–>(tyrosine hydroxylase)
  2. L-dopa–>(dopa decarboxylase)
  3. dopamine–>(dopamine beta-hydroxylase)
  4. norepinephrine–>(phenylethanolamine-N-methyltransferase in the adrenal medulla)
  5. epinephrine
120
Q

Serotonin
Location
Formation

A

Location: brainstem
Formed from tryptophan
Converted to melatonin in the pineal gland

121
Q

Glutamate

A

= the most prevalent excitatory neurotransmitter in the brain

122
Q

Four subtypes of glutamate receptors

A

Three subtypes = ionotropic receptors (= ligand-gated ion channels), including the NMDA receptor
One subtype = metabotropic receptor = coupled to ion channels via a heterotrimeric G protein

123
Q

GABA

A

= an inhibitory neurotransmitter

124
Q

GABA synthesis

A

from glutamate by the enzyme glutamate decarboxylase

125
Q

Two types of GABA receptors

A
  1. GABA-A receptor = increases Cl conductance

2. GABA-B receptor = increases K+ conductance

126
Q

Site of action of benzodiazepines and barbiturates

A

GABA-A receptor

127
Q

Glycine
Location
MOA

A

= an inhibitory neurotransmitter
Location: spinal cord, brainstem
MOA: increase Cl- conductance

128
Q

Nitric oxide (NO)
Location
Synthesis
MOA

A

= short-acting inhibitory neutrotransmitter
Location: GIT, blood vessels, CNS
Synthesis: presynaptic nerve terminals by NO synthase, which converts arginine–>citrulline and NO
MOA = permeant gas that diffuses from the presynaptic terminal to its target cell

129
Q

Sarcomere length

A

= from z line to z line

130
Q

Thick filament location and contents

A

present in the A band in the center of the sarcomere; contain myosin

131
Q

Myosin structure

A

6 polypeptide chains, including 1 pair of heavy chains and 2 pairs of light chains; each myosin molecule has 2 “heads” attached to a single tail

132
Q

Thin filament location and contents

A

present in the I bands; anchored at the Z lines; interdigitate with the thick filaments in a portion of the A band; contain actin, tropomyosin, and troponin

133
Q

Troponin

A

= the regulatory protein that permits cross-bridge formation when it binds Ca2+

134
Q

Structure of troponin

A

= a complex of 3 globular proteins

135
Q

Troponin T

A

T for tropomyosin; attaches the troponin complex to tropomyosin

136
Q

Troponin I

A

I for inhibition; inhibits the interaction of actin and myosin

137
Q

Troponin C

A

C for Ca2+; the calcium binding protein that, when bound to calcium, permits the interaction of actin and myosin

138
Q

T tubules

A

= extensive tubular network, open to the extracellular space, that carry the depolarization from the sarcolemmal membrane to the cell interior

139
Q

T tubule location

A

= junctions of A bands and I bands

140
Q

T tubule structure

A

Contain dihydropyridine receptors = a voltage sensitive protein that when depolarization occurs–>conformational change in the dihydropyridine receptor

141
Q

Sarcoplasmic reticulum (SR)

A

= the internal tubular structure that is the site of storage and release for excitation-contraction coupling

142
Q

Sarcoplasmic reticulum structure

A

Terminal cisternae that make intimate contact with the T tubules in a triad arrangement; contains the following:

  1. Ca2+-ATPase (calcium pumps)
  2. calcium loosely bound to calsequestrin
  3. calcium release channel = the ryanodine receptor
143
Q

Calcium pump

A

= Ca2+ -ATPase; transports calcium from the intracellular fluid into the SR interior, keeping the intracellular [Ca] low

144
Q

Steps in excitation-contraction coupling in skeletal muscle

A
  1. action potential depolarizes the T tubules
  2. conformational change in dihydropyridine receptor–>
  3. opening of ryanodine receptor (Ca release channels) in the SR
  4. release of Ca from the SR into the intracellular fluid
  5. increase intracellular Ca2+ concentration
  6. Ca2+ binds to troponin C on the thin filament–>conformational change that moves tropomyosin out of the way
  7. cross-bridge cycling
  8. reaccumulation of Ca into the SR via the SERCA
  9. Ca is released from troponin C
  10. tropomyosin again blocks the myosin binding site on actin and the muscle relaxes
145
Q

Steps of cross-bridge cycling

A
  1. no ATP bound to myosin–>myosin is tightly attached to actin (permanent rigor)
  2. ATP binds to myosin–>conformational change that causes myosin to be released from actin
  3. myosin is displaced toward the plus end of actin
  4. hydrolysis of ATP–>ADP + inorganic phosphate (Pi); ADP remains attached to myosin
  5. cycle repeats as long as calcium is bound to troponin C
146
Q

Mechanism of tetanus

A

Muscle is stimulated repeatedly before Ca2+ is released from the SR–>cumulative increase in intracellular Ca–>extending time of cross-bridging

147
Q

Isometric contractions

A

= length held constant; muscle length (preload) is fixed, muscle is stimulated to contract, and developed tension is measured - no muscle shortening

148
Q

Isotonic contractions

A

= load is constant; load against which the muscle contracts (afterload) is fixed, the muscle is stimulated to contract, and shortening is measured

149
Q

Length-tension relationship

A

= measures tension developed during isometric contraction when the muscle is set to fixed lengths (preload)

150
Q

Passive tension

A

= the tension developed by stretching the muscle to different lengths

151
Q

Total tension

A

= the tension developed when the muscle is stimulated to contract at different lengths

152
Q

Active tension

A

= the difference between total tension and passive tension; proportional to the number of cross-bridges formed

153
Q

Time of maximal tension

A

= when there is maximum overlap of thick and thin filaments; when the muscle is stretched to greater lengths, the number of cross-bridges is reduced because there is less overlap

154
Q

Force-velocity relationship

A

= measures the velocity of shortening of isotonic contractions when the muscle is challenged with different afterload (the load against which the muscle must contract); the velocity of shortening decreases as the afterload increases

155
Q

Structure of smooth muscle

A

Thick and thin filaments are NOT arranged in sarcomeres; therefore, they appear homogeneous rather than striated

156
Q

Types of smooth muscle

A
  1. multiunit smooth muscle
  2. unitary (single-unit) smooth muscle
  3. vascular smooth muscle
157
Q

Multiunit smooth muscle location

A
  1. iris
  2. ciliary muscle of the lens
  3. vas deferens
158
Q

Multiunit smooth muscle features

A
  1. behave as separate motor units
  2. little or no electrical coupling btwn cells
  3. densely innervated - contraction is controlled by neural innervation (e.g. autonomic nervous system)
159
Q

Unitary (single-unit) smooth muscle location

A
  1. GIT
  2. uterus
  3. bladder
  4. ureter
160
Q

Unitary (single unit) smooth muscle properties

A
  1. MOST COMMON type of smooth muscle
  2. spontaneously active (exhibits slow waves) and exhibits pacemaker activity
  3. high degree of electrical coupling between cells, and therefore, permits coordinated contraction of the organ (e.g. bladder)
161
Q

Two factors that control pacemaker activity

A
  1. hormones

2. neurotransmitter

162
Q

Vascular smooth muscle properties

A

Properties of both multiunit and single-unit smooth muscle

163
Q

Major difference btwn skeletal and smooth muscle excitation-contraction coupling

A

No troponin in smooth muscle - instead calcium regulates myosin on the thick filaments

164
Q

Steps of excitation-coupling in smooth muscle

A
  1. depolarization–>opening of voltage-gated calcium channels–>calcium flows into the cell down its electrochemical gradient–>
  2. increase in intracellular calcium concentration
  3. calcium binds to calmodulin
  4. calcium-calmodulin complex binds to and activates myosin light chain kinsae
  5. myosin light chain kinase phosphorylates myosin, allowing the myosin to bind to actin
  6. cross-bridge cycling
  7. decrease in intracellular calcium concentrations–>relaxation
165
Q

Mechanism of opening of ligand-gated calcium channels in smooth muscle cells

A

hormones and neurotransmitters–>directly release calcium from the SR through inositol 1,4,5-triphosphate (IP3-gated calcium channels

166
Q

Duration of action potential:
skeletal muscle
smooth muscle
cardiac muscle

A

Skeletal muscle = 1 msec
Smooth = 10 msec
Cardiac = 150msec (SA node, atria); 250-300msec purkinje fibers and ventricles

167
Q

Molecular basis for contraction btwn the three muscle types

A 
Skeletal = Ca2+-troponin C
Smooth = Ca2+-calmodulin increases myosin light chain kinase
Cardiac = Ca2+-troponin C

ACVIM General Boards (3 decks)

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