Studydroid is shutting down on January 1st, 2019

by mtoom

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Where is smooth muscle located?
On "hollow organs":
  • Vascular
  • GI (gastrointestinal)
  • Urogenital
  • Pulmonary
  • Glandular
  • Eye
  • Sphincters¬†
What sort of differences are there between smooth muscles?

These things are different:
  • Electrical activation
  • Receptors that are expressed
  • G proteins and effectors
  • Mechanotransduction
  • Extent and position of sarcoplasmic reticulum (SR)
What is reactive (or "functional") hyperemia?
The ability of muscle to respond to local needs (e.g. pH, O2, CO2) by relaxing after flow is briefly reduced or interrupted. This helps to restore blood flow quickly.
What does the myogenic response do for muscle?
It maintains flow by adjusting itself.
Where are filaments anchored in smooth muscle?
Dense bodies
Does smooth muscle have troponin?
How does Ca2+ activate myosin if there is no troponin?
What happens to MLCK (myosin light chain kinase) when it is bound by calmodulin?
It can become active, phosphorylating mysoin, allowing it to bind actin
Does removing Ca2+ from myoplasm stop contraction in smooth muscle? Why or why not?
No. Myosin is still covalently phosphorylated.
What does MLCK do?
It activates myosin by phosphorylating it
What does MLCP do?
It deactivates myosin by dephosphorylating it
When MLCP dephosphorylates mysoin when the myosin is bound to actin, what happens?
It continues the process of contraction, but does so at a much lower speed (~20 fold).
Does smooth muscle always have some level of tone?
What is the significance of having both MLCK/MLCP in terms of maintaining tone?
Phosphorylating/dephosphorylating will result in much bound myosin being dephosphorylated. This means that it will contract more slowly, having the result of using less ATP while maintaining tone.
Why does smooth muscle always have some tone?
Ca2+ levels and MLCK/MLCP enzymes
What causes the phosphorylation of MLCK (thereby inactivating it) and promoting relaxation?
  • Protein Kinase A (due to beta-agonists)
  • Protein Kinase G (due to ANP, NO)¬†
What causes the phosphorylation of MLCP (thereby inactivating it) and promoting contraction?
  • Rho Kinase (Norepinephrine, angiotensin II, endothelin-1)
What is meant by pharmacomechanical coupling with regard to smooth muscle?
The chemical signals that affect contraction do not in any way effect the Em of the smooth muscle cell.
Do smooth muscles need Ca2+ to enter the cell to contract?
What receptor is found on SR of smooth muscle?
How does calcium get out of SR in smooth muscle?
CICR (calcium-induced calcium-release)
Is resting calcium level in smooth muscle higher or lower than skeletal muscle?
What 2 things does the sympathetic nervous system release to stimulate contraction of smooth muscle?
  • ATP
  • Noradrenaline
How is calcium allowed into the cell to stimulate contraction (i.e. by what mechanism does intracellular calcium go up)?
  • ATP - opens ATP-gated Ca2+¬†channel
  • Noradrenaline, ATII, ET1 - cause conversion of PIP2 to DAG and IP3, promoting release of Ca2+ from myoplasm
How is calcium removed from myoplasm?
  • Activation of PKA and PKG causes activation of phospholamban
  • Phospholamban stimulates ATPase to restore Ca2+ into SR lumen from myoplasm
What are the 2 mechanisms that PKA and PKG use to cause relaxation of smooth muscle?
1. Activate ATPase via phospholamban
2. Phosphorylate MLCK, promoting relaxation
What are the 2 mechanisms that Rho Kinase uses to cause contraction of smooth muscle?
1. Release Ca2+ via IP/DAG
2. Phosphorylate MLCP, promoting contraction
What is a single unit smooth muscle cell?
It is connected by gap junctions to other cells, allowing more coordinated contraction.
Do smooth muscles have a motor endplate? What do they have instead?
No, they have varicosities that spread neurotransmitter into the interstitial space.
What are multi unit smooth muscle cells?
Smooth muscle cells with no gap junctions. Every cell operates independently.
What does preganglionic parasympathetic neurons do with acetylcholine at synapses with varicosities?
Acetylcholine reduces release of noradrenaline from varicosities
What causes functional hyperemia?
Low O2, High CO2, Low pH
What is the result of ATP levels going low within myoplasm of smooth muscle?
Opening an ATP-gated potassium channel, that depolarizes cell and allows it to relax.
What is the result of Ca2+ levels going high within myoplasm of smooth muscle?
Opening a K-gated potassium channel, that depolarizes cell and allows it to relax.
What is the fast response (as a result of NE and ATP released from varicosity)?
  • ATP opens ligand-gated channel, allows Ca2+ and Na+ to enter
  • Depolarization opens voltage-gated Ca2+ channels
  • RyR2 opens (CICR), MLCK activated - Tone increases
  • NE binds alpha-1, activates phospholipase C giving you IP/DAG
What happens after fast response?
  • SR and PM ATPases begin to restore Ca2+
  • IP3 binds its SR receptor, release Ca2+ and contributing to MLCK activation (helps to sustain contraction)
  • Rho kinase inhibits MLCP

Finally, ATP/NE removed, 2nd messengers return to pre-stimulation levels and tone goes down
Binding of purinurgic receptor by ATP allows what into the cell?
x of y cards