9 - Smooth muscles physiology Flashcards

1
Q

G actin molecules form a chain of ________,

and 2 of them will form a double-helical actin chain.

A

F actin

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2
Q

_________ is absent from the thin filament of the smooth muscle. Instead, ______ is used as the regulatory protein that binds Ca2+.

A

Troponin;
Calmodulin

  • in skeletal muscles, TnC complex is formed (Troponin bound to Ca2+)
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3
Q

In smooth muscles, there is

A. regular arrangement of protein filament
B. sarcomere
C. no striation

A

C only

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4
Q

In smooth muscles,
A. there is more actin than myosin
B. actins are much longer and therefore myosin can slide a longer distance without encountering the end of sarcomere.
C. the degree of shortening is greater than skeletal muscles

A

All of them are correct

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5
Q

In smooth muscles, why is extracellular Ca2+ so important?

A

Absence of T tubule system, thus less extensive sarcoplasmic reticulum.

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6
Q

A large number of ___________ are prevent for increasing SA for Ca2+ influx.

A

Caveolae

small membrane infoldings

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7
Q

What are the 4 extracellular sources and 2 intracellular sources of Ca2+ for contraction?

A

Extracellular
1. Voltage-gated Ca2+ channel (L-type Ca2+ channel)

  1. Ligand-gated Ca2+ channel
  2. Stretch-sensitive Ca2+ channel (non-selective cation channel)
  3. Stored-operated Ca2+ channel

Intracellular
5. IP3-gated Ca2+ channel

  1. Ca2+-gated Ca2+ channel (Ryanodine receptor for Ca2+ -induced Ca2+ release)
    (ryanodine is a drug that opens this channel)
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8
Q

What is the mechanism of smooth muscle contraction?

5 steps

A
  1. Intracellular Ca2+ concentrations increase when Ca2+ enters the cell / released from SR
  2. Ca2+ binds to calmodulin
  3. Ca-calmodulin activates myosin light chain kinase (MLCK)
  4. MLCK phosphorylates light chains in myosin heads to trigger binding of myosin head to actin(by increasing affinity of myosin head to actin) and increases myosin ATPase activity
  5. Active myosin cross bridges along actin and create muscle tension
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9
Q

Why does smooth muscles have a slower onset time of contraction?

A

Phosphorylation of the myosin light chain is kinase is needed.

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10
Q

Considering muscle relaxation, transport proteins responsible for lowering cycstolic ca2+ include:

A
  1. Plasma membrane Ca2+ - ATPase (PMCA)
  2. Sarcoplasmic reticulum Ca2+ -ATPase (SERCA)
  3. Na+/Ca2+ exchanger (NCX)
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11
Q

The dephosphorylated cross-bridge is known as _______.

A

Latch bridge

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12
Q

Slower onset rate and offset rate of smooth muscles compared to cardiac and skeletal muscles due to?

A
  1. More complicated electro-mechanical transduction system
    (requires Ca2+ calmodulin to activates MLCK and phosphorylation of MLCK )
  2. Slower ATPase activity
  3. Slower cycling rate (ADP)
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13
Q
Tonic contraction:
A. contract most of the time
B. Rhythmic contraction in response to stimuli (AP)
C. Effectors: GI muscles, uterus 
D. Multi-unit muscles
E. Pharmacomechanical coupling
A

A, D and E only

B: relax in responses to inhibitory signals

C. Effectors: Sphincter, arterial smooth muscles, air way

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14
Q
Phasic contraction:
A. relax most of the time
B. Rhythmic contraction in response to stimuli (AP)
C. Effectors: GI muscles, uterus 
D. Single unit muscles
E. Electro-mechanical coupling
A

All correct

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15
Q

What is pharmacomechanical coupling (by tonic contraction)

and

electromechanical coupling (by phasic contraction)

and

mechano-mechanical coupling

respectively?

A

Electromechanical:
Slow wave potential > open L-type Ca2+ channel >Ca2+ induced Ca2+ release

Pharmacomechanical:
Cytosolic Ca2+ increases due to
a) release from intracellular store (PLC-IP3)

Binding to GPCR linked to Gq protein

  • > activation of phospholipase C (PLC)
  • > generation of IP3 and DAG.
  • > IP3 stimulates Ca2+ release from intracellular store.

;
b) entry through ligand-gated non-selective cation channels

PLC could be induced by Gq protein (adrenaline/NA/Ach)

Mechano-mechanical coupling:
Muscle is excited by stretch which opens stretch-sensitive Ca2+ channels

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16
Q

Mechanisms of producing smooth muscle relaxation?

A
  1. Dephosphorylation of myosin by myosin phosphatase (MP); MP is activated by fall in [Ca2+] or PKG
  2. Inactivation of MLCK by phosphorylation (cAMP-PKA)
  3. Lowering of [Ca2+] by PMCA, SERCA by phosphorylation (cGMP-PKG, cAMP-PKA)
  4. Blocking L-type Calcium channel by Verapamil, nifedipine, diltiazem.
  5. Hyperpolarization by K+ channel blocker (Cromokalim) by opening K+ channels ; or phosphorylation of K+ Channel by cAMP-PKA, cGMP-PKG
  6. Inhibition of Phosphodiesterase(PDE)> slower the breakdown of cAMP / cGMP to prolong their effects on PKA/ PKG

PDE can cause smooth muscle relaxation
*PDE-5 inhibitor: Used in treating erectile dysfunction by prolonging vasodilation