Smooth and cardiac muscle Flashcards

exam 3

1
Q

Smooth vs skeletal muscle: strength

A

smooth muscle is stronger per gram of muscle

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2
Q

Smooth vs skeletal muscle: efficiency

A

Smooth muscle is more efficient and has greater variability

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3
Q

Smooth vs skeletal muscle: speed

A

Smooth muscle is slower due to slower cross-bride cycling

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4
Q

Smooth vs skeletal muscle: % of body mass

A

Smooth muscle is 10% of body weight; skeletal muscle is 40% of body weight

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5
Q

Smooth vs skeletal muscle: actin-myosin ratio

A
  • Actin-myosin arrangement is less orderly than skeletal muscle (2:1)
  • Larger proportion of actin in smooth muscle (10-20:1)
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6
Q

Smooth vs skeletal muscle: anchor

A

smooth muscle - dense bodies
skeletal muscle - z discs

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7
Q

Smooth vs skeletal muscle: SR

A

SR in smooth muscle is less developed - more dependent on outside Ca++ coming into cell because less Ca++ in SR

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8
Q

______ allows smooth muscle to maintain force of contraction for a long time while using minimal energy

A

“Latch” mechanism

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9
Q

Smooth vs skeletal muscle: myosin anatomy

A
  • smooth - gap between myosin - allows greater shortening/stretching; heads pointed in opposite directions
  • skeletal muscle has minimum shortening - no gap between myosin
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10
Q

Smooth vs skeletal muscle: shortening

A

smooth - half the size
skeletal - ~2cm

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11
Q

Smooth vs skeletal muscle: NT response

A

smooth: relax or contract (depends on receptor)
skeletal: contraction

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12
Q

What are the ways that Ca++ enters the cells for smooth muscle

A

leak channels
voltage-gated (L-type)
ligand-dependent

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13
Q

If Ca++ is 0, there will be no ____

A

BP - heart won’t work and no contraction bc it’s dependent on outside Ca++

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14
Q

most smooth muscle is _____ smooth muscle

A

visceral or unitary

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15
Q

Compare unitary (visceral) to multi-unit smooth muscle

A

Visceral/unitary - most of smooth muscle; gap junctions - coordinated contraction (intestines)

Multi-unit smooth muscle - no pathway for ions to move between neighboring cells - more graded (delicate) control; entirely dependent on NTs being released in area - ciliary and iris muscles in eye

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16
Q

The ______ is the only hybrid smooth muscle in the body

A

esophagus - has both unitary and multi-unit smooth muscle

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17
Q

Describe the 3 layers of the blood vessels

A
  1. Tunica Intima - endothelial (one layer thick) - capillaries
  2. Tunica Media - smooth muscle, middle layer
  3. Tunica Adventitia/Externa - Adventitia/outside layer; structural support
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18
Q

NO is produced in the _____

A

endothelium

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19
Q

In skeletal muscle, the NT is always ___

A

ACh

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20
Q

In smooth muscle, ACh causes ______ in the vasculature

A

relaxation

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21
Q

In smooth muscle, ACh causes ______ in the small intestine

A

contraction

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22
Q

Pacemaker cells have higher resting membrane permeability to _____ or ______

A

Na+(#1) or Ca++(#2)

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23
Q

Differentiate between the role of tropomyosin in smooth vs skeletal muscle

A

In skeletal muscle, tropomyosin gets in the way of myosin head being able to bind to active sites
In smooth muscle, active sites are always exposed (tropomyosin still there, but doesn’t do anuything)

24
Q

The regulation of smooth muscle is determined by ______

A

myosin filaments - regulatory light chain, requires phosphorylation

25
Q

Ca++ can be removed from the smooth muscle cell via

A
  • SERCA - back into SR
    To ECF:
  • Plasma membrane Ca++ ATPase (PMCA)
  • NCX - 3 Na+ in for 1 Ca+ out
26
Q

What determines MLCK activity?

A

Amount of Ca++ in cell (calmodulin binding)

27
Q

Ca++ binds to _____ to activate MLCK

A

calmodulin

28
Q

Voltage gated Ca++ channels in smooth muscle are ___ type

A

L

29
Q

Myosin ______ adds a phosphate to myosin, while myosin _____ removes phosphate from myosin

A

MLCK - activates
phosphatase - inactivates

30
Q

What are the two things that PKG can phosphorylate? What is the result?

A
  • MLCK - reduces activity
  • Ca++ entry channels - closes channels
31
Q

What are the effects of NO in the vascular smooth muscle cell?

A

Increases activity of guanylyl cyclase - more cGMP - more relaxation through increased phosphatase activity of MLC or increased activity of PKG

32
Q

How is NO made?

A

Endothelial cells turn arginine into NO via eNOS (endothelial NO synthase)

33
Q

How can the activity of MLKC be reduced?

A
  • remove the Ca++
  • NO
34
Q

How is eNOS activity increased?

A

neurotransmitters - ACh and bradykinin release Ca++ from their ER, interacts with calmodulin → increases activity of ENOS

35
Q

How is cGMP inactivated?

A
  • eventually falls apart (unstable)
  • phosphodiesterase
36
Q

How can you prolong the life of cGMP?

A

Phosphodiesterase inhibitor - sildenafil

37
Q

Sildenafil was originally made to treat _______

A

pulmonary HTN

38
Q

_____ is the only NT that can constrict brain blood vessels. What is the mechanism?

A

5-HT - binds to alpha 1 receptor

39
Q

Describe the effects of an agonist binding to an alpha 1 receptor on a vascular smooth muscle cell

A

Increased PLC (phospholipase C) → cleaves a PG into DAG and IP3
- IP3 releases Ca++ from the SR → contraction
- DAG activates PKC → contraction

40
Q

How can SSRIs treat headaches?

A

Reduce swelling in head via vasoconstriction

41
Q

How can contraction of smooth muscle occur without an AP?

A
  • Ca++ leaking into cell
  • manipulation of the pathway via signaling compound
42
Q

Discuss the different smooth muscle AP possibilities

A

Normal AP
Slow, rhythmic waves - pacemaker
AP with plateau - L type Ca++ channels, uterus

43
Q

In heart muscle, where does the Ca++ that triggers an AP come from? How does this happen?

A

the SR - well developed
Ca++ induced Ca++ released - comes from outside initially

44
Q

In heart muscle how much of the Ca++ comes from the SR vs ECF for an AP?

A

80% from SR
20% from ECF

45
Q

Differentiate between T-type and L-type Ca++ channels

A

T-type - fast
L-type - slow

46
Q

What is the trigger for Ca++ channels to open in a heart cell?

A

AP - Na+ entry

47
Q

Where does the Ca++ come from that enters heart cells to trigger contraction?

A

T-tubules

48
Q

How is the Ca++ removed from the heart cell after contraction?

A

Ca++ removed by SERCA pump (80%), remainder is removed from cell via NCX (primary, 15%) or plasma membrane Ca++ ATPase (PMCA) pump (5%) - towards end of Ca++ removal (low levels of ICF Ca++)

49
Q

_______ is the Ca++ sequestering protein

A

Calsequestrin - a sequestering protein - takes something out of circulation (Ca++) and allows concentrated storage of Ca++ in the SR

50
Q

Calsequestrin is found in ____ muscle cell with a SR

A

any

51
Q

_______ is the inhibitor of the SERCA pump in the heart

A

Phospholamban - allows Ca++ to stay in sarcoplasm longer → more contraction from muscle

52
Q

Phospholamban is only found in the _______

A

heart cells

53
Q

Inhibition of Phospholamban would do what?

A

shorter length of contraction and faster resetting; increased HR

54
Q

Differentiate between cholinergic and adrenergic activity in the heart

A

adrenergic - stronger/faster contraction
cholinergic - slower/weaker contraction

55
Q

Discuss the modulation of cholinergic and adrenergic activity in the heart

A

cAMP dependent
- Beta activity → adenylyl cyclase → ATP → cAMP → PKA → stronger strength of contraction and HR
- mACh receptor activity - reduced cAMP production→ reduces activity of PKA → slower HR and weaker contractions