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FBS1 > PPP - muscles > Flashcards

PPP - muscles Flashcards

1
Q

What are the t tubules?

A

invaginations of the sarcolemma on myofilaments at every Z line

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2
Q

What is the function of t tubules?

A

bring the action potential deep into cells to ensure coordinated contraction

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3
Q

What are the terminal cisternae?

A

intracellular bags of membrane that store calcium - lie underneath the t tubules

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4
Q

What are triads and dyads?

A

Triads are in skeletal muscle, dyads in cardiac

- they are the SR - t tubule interface

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5
Q

What connects neighbouring cardiac cells?

A

intercalated discs

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6
Q

What are some features of the cardiac action potential?

A

Influx due to Ca2+ and Na+
long duration - 200-400ms
length decreases if heart rate goes up

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7
Q

What is the purpose of the long cardiac action potential?

A

prevents tetany

prevents agains re-entrant arrhythmias

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8
Q

What is the main difference between cardiac and skeletal initiation of contraction?

A

Ca2+ release is driven by voltage in skeletal muscle

Ca2+ release is driven by a small Ca2+ influx in cardiac muscle

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9
Q

What are the Ca2+ receptors on t tubules called?

A

DHP receptors

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10
Q

What type of receptors are used to release Ca2+ from the SR?

A

RyR receptors

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11
Q

What are the steps of excitation-contraction coupling in cardiac muscle?

A
  1. AP travels into cell via t tubules
  2. DHP receptors are activated to allow small influx of Ca2+
  3. Ca2+ binds RyR on SR to induce large Ca2+ release
  4. Ca2+ can now activate myofilaments to contract
  5. Ca2+ is removed by SERCA and Na/Ca exchanger
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12
Q

How does Ca2+ activate contraction in cardiac muscle?

A

it binds to troponin C

this pulls tropomyosin out of the way to allow cross-bridge formation

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13
Q

What is the length-tension relationship in cardiac muscle?

A

increased stretch in cardiac muscle causes increased force of contraction

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14
Q

What 2 factors contribute to the cardiac length-tension relationship?

A
  • increased sarcomere length causes increased cross-bridge overlap
  • increasing length increases sensitivity of troponin C to Ca2+
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15
Q

What is the force-frequency relationship in cardiac muscle?

A

increasing rate of contraction leads to increased force

- also get increased Ca2+ influx

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16
Q

What happens to the force-frequency relationship in heart failure?

A

get a negative effect (increased rate decreases force)

  • as SERCA is down-regulated and Na/Ca exchange is up-regulated
  • get reduced ca concentration
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17
Q

What is the maximal/optimal sarcomere length for cardiac muscle?

A

2.25uM

18
Q

What are the main features of smooth muscle cells?

A
  • elongated
  • non-striated
  • actin fillaments are anchored by dense bodies
  • dense bodies are connected by intermediate filaments
  • communicate through gap junctions
  • higher actin:myosin ration than other muscle
19
Q

In what types of smooth muscle is an action potential not always needed for contraction?

A

airways and sometimes vascular

20
Q

What stimulates contraction in intestinal smooth muscle?

A

interstitial cells of cajal

21
Q

What stimulates contraction in myometrium smooth muscle?

A

intrinsic rhythm

22
Q

What can cause Ca2+ release from the SR in smooth muscle?

A
  • IP3
  • VGCC opening
  • receptor gated channel opening
23
Q

What are some vasoconstriction factors?

A 
noradrenaline (main)
pressure/stretch
adrenaline
angiotensin II
local hormones
24
Q

What are some vasodilating factors?

A

NO (released from endothelial cells
low pH
tissue metabolites
local hormones

25
Q

What is the main method of vascular smooth muscle contraction?

A
  • Via VGCC opening:
    1. Noradrenaline binds alpha 1 receptors
    2. activates PLC and Rho kinase
    ( Rho kinase causes Ca2+ sensitisation)
    3. PLC cleaves PIP2 -> DAG + IP3
    4. IP3 releases Ca2+ from SR
    5. DAG opens RGC membrane channels to get Na+ and Ca2+ influx
    6. leads to membrane depolarisation
    7. VGCC becomes activated and causes large Ca2+ influx
26
Q

What is an alternative method of vascular smooth muscle contraction?

A

stretch activates ion channels

  • get Na+ influx
  • membrane depolarisation
  • VGCC open
27
Q

How does vascular smooth muscle actively relax?

A

Via No or cAMP

28
Q

How does NO-mediated SM relaxation occur?

A
  • NO diffuses into cell and activates guanylate cyclase
  • GTP -> cGMP

cCMP has several effects:

  1. causes Ca2+ desensitisation
  2. activates K+ channels to cause hyperpolaisation -> VGCC close
  3. activation of SERCA and PMCA
29
Q

How does cAMP mediated SM relaxation occur?

A
  • adrenaline binds beta 1 receptors
  • activates adenylate cyclase
  • ATP -> cAMP

cAMP has 2 effects:

  1. K+ channel opening -> depolarisation
  2. SERCA and PMCA activation
30
Q

How do smooth muscle fibres prevent fatigue?

A
  • lower ATP requirement due to slow cross-bridge cycles

- possibly via latch bridge formation

31
Q

How does the myosin kinase complex become activated?

A

calmoduin binds 4Ca2+

combines with myosin light chain kinase

32
Q

How is myosin regulated in smooth muscle?

A

activated (phosphorylated) by myosin kinase -> can form cross bridges
dephosphorylated by myosin phosphatase

33
Q

How does Ca2+ sensitisation occur?

A

rho kinase causes inhibition of myosin phosphatase -> less myosin is inactivated

34
Q

How does Ca2+ desensitisation occur?

A

NO -> cGMP
cGMP activates myosin phosphatase
- more myosin is inactivated by dephosphorylation

35
Q

What happens to myosin regulation when Ca2+ is removed?

A

the calmoduin-kinase complex falls appart

- all remaining active myosin is dephosphorylated by myosin phosphatase

36
Q

What is latch-bridge formation?

A
  • theory to explain low ATP requirement of smooth muscle
  • form when myosin is inactive but still bound to actin
  • cycle very slowly to maintain force
37
Q

What are slow waves?

A

spontaneous oscillations of smooth muscle which lead to depolarisation
- can be generated by pacemaker cells or SMCs themselves

38
Q

What is the main cause of action potentials in smooth muscle?

A

VGCC opening

39
Q

What is the main cause of relaxation in smooth muscle?

A

hyperpolarisation

40
Q

What is the difference between multi-unit and unitary smooth muscle?

A

multi-unit = each SMC has synpatic input (allows finer control)

unitary = some SMCs are innervated and impulse spreads through gap junctions (allows coordination)

FBS1 (9 decks)

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