Smooth Muscle (Exam III) Flashcards Preview

A&P I (Fall 2022) > Smooth Muscle (Exam III) > Flashcards

Flashcards in Smooth Muscle (Exam III) Deck (47)
Loading flashcards...
1
Q

What are smooth muscle cells lengths compared to skeletal muscle?
Do smooth muscle cells have a sarcomere?
Are smooth muscle cells attached to theskeleton?

A
  • Shorter than skeletal muscle
  • No
  • No
2
Q

What is the actin:myosin ratio of smooth muscle?
How does this compare to skeletal muscle?

A
  • Smooth = 10 actin : 1 myosin
  • Skeletal = 2 actin : 1 myosin
3
Q

What functions as a replacement for the Z-disk in smooth muscle?
What is this structure made of?

A
  • Dense Bodies
  • Dense Bodies are made of collagen.
4
Q

What is stronger, smooth muscle or skeletal muscle? How much more so?

A

Smooth muscle is 2x stronger per 100grams

5
Q

How does the energy usage of smooth muscle compare to that of skeletal muscle?

A
  • Smooth muscle is much more efficient
  • 1/10 to 1/300 energy usage compared to skeletal muscle.
6
Q

How does the speed of contraction of smooth muscle compare to that of skeletal muscle?

A
  • Smooth muscle: 0.5 - 2 sec contraction speed
  • Skeletal muscle: 0.15ms contraction speed
7
Q

Where is actin anchored in smooth muscle cells?
Where are dense bodies located in smooth muscle cells?
How do smooth muscle cells connect to other smooth muscle cells?

A
  • Dense bodies
  • Dense bodies are attached to the cell wall.
  • Smooth muscle cells attach to each other through their dense bodies.
8
Q

Where do neurotransmitters send signals to trigger Ca⁺⁺ release in smooth muscle cells?
How does the sarcoplasmic reticulum of smooth muscles compare to that of skeletal muscle?

A
  • Caveolae
  • Smooth Muscle SR is limited comparatively and hangs out at the caveolae.
9
Q

How much internal Ca⁺⁺ do smooth muscle cells store?
What does this mean clinically?

A
  • Very little compared to skeletal muscle (depending on Ca⁺⁺ concentration of ECF)
  • Hypocalcemia = ↓ BP due to ↓ SVR from smooth muscle’s inability to constrict.
10
Q

Which “state” of cross-bridge cycling lasts longer in smooth muscle than skeletal muscle? Why?

A
  • Released State
  • Tension is maintained by myosin head holding on to actin longer even with ATP present.
11
Q

Where might we see smooth muscle cells in the body?

A

GI system, ciliary muscle, GU tract, uterus

12
Q

What is required for release of the myosin head from the actin in smooth muscle vs skeletal muscle?

A
  • Skeletal Muscle: ATP binding to myosin head causes myosin head to detach from actin.
  • Smooth Muscle: MLCP needed to dephosphorylate for myosin head to release.
13
Q

How much more quickly do skeletal muscle contractions take place than smooth muscle contractions?

A

Skeletal muscle is 10 - 300 times faster.

14
Q

To what degree can smooth muscle shorten its length? How does this compare to skeletal muscle?

A
  • Smooth muscle: 80% of length shortening capability.
  • Skeletal muscle: 30% of length shortening capability.
15
Q

What structure of the skeletal muscle prevents length shortening to the same degree as the smooth muscle?

A

Skeletal muscle Z-disks

16
Q

What are the two classifications of smooth muscle cells? Where are each found?

A
  • Visceral (Unitary): larger organs (GI, GU, Blood vessels, resp, etc.)
  • Multi-Unit: Ciliary muscles of the eye. (anywhere that fine control is needed)
17
Q

What organ is unique in its composition of both smooth muscle and skeletal muscle?

A

Esophagus

18
Q

What differentiates Visceral smooth muscle and Multi-unit smooth muscle?

A

Unitary (Visceral) Smooth muscle:
- Intercellular communication via gap junctions
- More common
Multi Unit Smooth Muscle:
- Insulated via glycoprotein fibrous coating
- No cell-cell communication
- Fine graded control

19
Q

What are the layers of an artery (superficial to deep) and their alternate names?

A
  • Tunica Externa (Adventitia)
  • Tunica Media (Smooth muscle layer)
  • Tunica Intima (Endothelium)
20
Q

What is the composition of the Adventitia? How does this differ in arteries and veins?

A

Adventitia is composed of connective tissue.
- Arteries have more connective tissue (elastin) resulting in more resilience.
- Veins have less elastin and less resiliency.

21
Q

How large is the endothelial layer of blood vessels?
How dependent is CV health on this layer?
What occurs with a diseased endothelium?

A
  • 1 cell layer thick
  • CV health is very dependent on the health of the endothelium.
  • Blood vessels can’t dilate as well with a damaged endothelium.
22
Q

How many layers of tissue do capillaries have?

A

One layer (Endothelium)

23
Q

Which muscle cell type is able to “relax” more?

A

Smooth Muscle Cells

24
Q

What is general Vᵣₘ for skeletal muscle?

A

-80mV

25
Q

What troponin molecules does smooth muscle have?

A

None

26
Q

Ca⁺⁺ combines with what molecule to activate MLCK?

A

Calmodulin

27
Q

How does MLCK cause contraction?

A

Through phosphorylation of regulatory chain of Myosin molecule → Contraction.

28
Q

What types of Ca⁺⁺ channels can influx Ca⁺⁺ in smooth muscle?

A
  • Ligand-gated Ca⁺⁺ Channels
  • VG Ca⁺⁺ Channels
  • Leaky Ca⁺⁺ Channels
29
Q

How does smooth muscle relaxation differ from smooth muscle contraction?

A
  • Relaxation means less Ca⁺⁺ intracellularly
  • ↓ Ca⁺⁺ ICF = No Calmodulin
  • No Calmodulin = No Phosphorylation
  • Myosin Phosphatase (MLCP) dephosphorylates Myosin Heads causing relaxation.
30
Q

What receptors, located on endothelium, can start the process of NO creation?

A

mACh GPCRs or Bradykinin GPCRs

31
Q

In an endothelial cell, what does the Ca⁺⁺CaM complex do?

A
  • Uses eNOS to convert Arginine → Nitric Oxide (NO)
32
Q

What conditions found in of lumen of the blood vessels cause endothelial cells to start producing more Nitric Oxide (NO) ?

A
  • ↑ Flow/ Shear Stress
33
Q

Nitric Oxide will dilate what primarily?

A

Veins (but has both arterial and venous activity)

34
Q

Nitrates & nitrites cause increases release of what?

A

Nitric Oxide (NO)

35
Q

Myosin Light Chain Kinase (MLCK) will do what to the regulatory chain of Myosin Light Chain?

A

Phosphorylate Myosin Light Chain causing cross-bridge cycling.

36
Q

What inactivates phosphorylated myosin light chain?

A

MLCP (Myosin Light Chain Phosphatase)

37
Q

Are action potentials always required for smooth muscle contraction? Why or why not?
What is an example of this concept?

A
  • No, an oscillating Vᵣₘ can cause smooth muscle contraction.
  • An example of this concept would be the “mixing” smooth muscles of the GI tract (Peristalsis?)
38
Q

Where are α1 receptors located in the brain?
What is the consequence of this?

A
  • No α1 receptors are in the brain.
  • The brain is not responsive to pressors.
39
Q

Where are α1 receptors not found in the CV system?

A
  • Brain
  • All capillaries
40
Q

What mechanism causes myogenic constriction in the brain?

A

Na⁺ & Ca⁺⁺ stretch receptors responding to ↑ stretch from ↑ MAP.

41
Q

What neurotransmitters are responsible for cerebral vasoconstriction/vasodilation?

A

Trick question. No NT’s, only Na⁺ & Ca⁺⁺ stretch receptors.

42
Q

What is an example of an inverse response of smooth muscle being stretched resulting in increased dilation of said smooth muscle?

A

Bladder response to filling with urine

43
Q

What does DAG do?
What is the result of this?

A
  • Activates PKC (protein kinase C)
  • PKC:
    1. Potentiates MLCK
    2. ↑ pCa⁺⁺
44
Q

What does IP₃ do?

A

IP₃ potentiates Ca⁺⁺ release by binding to Ca⁺⁺ channel receptors on the sarcoplasmic reticulum.

45
Q

What type of receptor is an α1 receptor?
What specific sub-type?

A
  • GPCR
  • Gₛ or Gq
46
Q

What does Phospholipase do?
What activates phospholipase?

A
  • PLC cleaves Phosphatidyl-Inositol to DAG & IP₃.
  • PLC is activated by the active α-subunit of the G-protein.
47
Q

What activates PKG?
What actions does PKG have?

A
  • PKG activated by cGMP
  • PKG potentiates MLCP & inhibits MLCK, causing relaxation.