Smooth Muscle Flashcards

1
Q

Where are the smooth (S) mm found?

A

although the variety and function of S mm is amazing. It mostly surrounds hollow organs (blood vessels, bronchi, gut, reproductive and urinary tracts) and are arranged in sheets

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2
Q

What are some of the functions of S mm?

A

Maintains pressure-circular layer in airways, blood vessels
Mix and Propel contents-circular and longitudinal layers in intestinal wall
Regulates internal flow-rectangular layer in bladder, rectum, small testicular duct

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3
Q

In terms of contractile elements, what are the 2 structures missing in S mm but present in C mm, and SK mm?

A

Troponin- instead they have Calponin and Caldesmon

T-Tubules

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4
Q

What are other unique characteristics of S mm?

A
  • Have calponin and caldesmon instead of troponin
  • Lack T-tubule
  • contain less developed SR
  • Dense areas (points of mechanical coupling) analogs to Z lines in striated mm
  • Gap junction (points of electrical coupling)
  • Thick and thin filaments organized diagonally
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5
Q

Where does Ca need for contraction come from?

A

Ca needed for contraction come from the extracellular space and SR unlike in SK mm where it solely comes from SR.

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6
Q

What is the difference b/n tonic and phasic contraction?

A

Tonic: maintain a continuous level of partial contraction (tone). Ex: walls of blood vessels, airways of the lungs, sphincters. NO AP needed to initiate contraction but affected by Em, not at elevated Ca, sustained stimulation
Phasic: contract rhythmically or intermittently in GI, reproductive, and urinary systems. NEED AP to initiate contraction, short stimulation

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7
Q

Label and understand Tonic and Phasic contraction figures.

A

pp. 6

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8
Q

T/F Unlike in cardiac mm, S mm need extracellular Ca for contraction.

A

F. Both need extracellular Ca influx that causes CICR from SR. But S mm also uses the release of IP3.

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9
Q

How does IP3 result in cytoplasmic [Ca] increase?

A
  • Agonist bind to Ca channels and activate a pathway that results in IP3 release.
  • IP3 goes to SR to stimulate IP3 R
  • Ca released from SR
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10
Q

Label/Study Sources of Ca for S mm contraction Figure

A

pp7

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11
Q

If S mm lack troponin, how does Ca control contraction in S mm?

A

Ca bind to calmodulin-Ca-calmodulin complex activates myosin light chain kinase (MLCK)-MLCK hydrolyzes ATP to phosphorylate inactive myosin-trigger crossbridge formation (Figure on pp. 8).

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12
Q

What is the Ca switch that turns on the contractile apparatus in S mm, and striated mm?

A

S mm: Ca dependent phosphorylation of MLC

Striated (C mm and SK mm): Ca binding to troponin

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13
Q

What is the rate-limiting step in S mm contraction?

A

Phosphorylation of the myosin head. Unlike SK mm, in S mm regulation of cross-bridge occurs on the thick filament.

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14
Q

Understand Figure showing rate limiting step.

A

pp. 9

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15
Q

T/F Myosin ATPase of S mm splits ATP at a much slower rate than SK mm.

A

T. S mm can generate more tension per unit of cross sectional area (Figure pp 10).

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16
Q

What induces S mm relaxation?

A
  • NO-PKG- inactivate MLCK
  • Epinephrine-PKA-inctivate MLCK
  • Myosin light chain phosphatase-dephosphorylate myosin head.
17
Q

Some types of S mm cells are self excitable (in the absence of hormonal and neural input). What are the processes they use for spontaneous excitation?

A

Pacemaker Potentials: spontaneous depolarization due to cationic current (mostly Na coming in)
Slow-wave Potentials: spontaneous hyperpolarizing and depolarizing swings (electrogenic pumps activity)

18
Q

The contractile activity of S mm can be controlled by numerous factors such as _____, _____, ______, and ______

A
  • Electrical Activity
  • Hormones
  • Autonomic Nerves
  • Drugs
19
Q

T/F Summation and tetanus take place in SK but not in S mm and C mm.

A

F. Summation and tetanus happen both in SK and S mm but not C mm.

20
Q

S mm cells produce a wide range of membrane potential (Vm) variations that can either initiate or modulate contraction. Mention 4 of these variations:

A
  • AP: twich, summation (E-C coupling)
  • Slow-waves with AP bursts at waves crests (E-C coupling)
  • Changes in Vm: chronic hyperpolarization and depolarization (E-C coupling with no AP)
  • Contractile activity with no changes in Vm: chemical influence (drugs and hormones) (Pharmaco-mechanical coupling).
21
Q

How does the ANS synapse on S mm cells differ from neuromuscular junction?

A

The postganglionic autonomic fibers travel across the surface of S mm cells. The varicosities will release neurotransmitter that will travel to neighboring S mm cells with adrenergic and cholinergic receptors. More wide spread and slow propagation of neurotransmitters.
NOTE: transmitter release modify rate and strength of activity.

22
Q

What are the two types of S mm based on electrical characteristics of their plasma membrane?

A

1) Multi-Unit

2) Single Unit

23
Q

What cells resemble Multi-unit and single-unit S mm?

Study Figure pp19

A

1) Multi-Unit- resemble SK mm b/c no electrical coupling (lack gap junction), & neuronal regulation is important.
2) Single-unit-resemble C mm b/c electrical activity is propagated via gap junctions

24
Q

Mention some of the hormones and neurotransmitters that modulate the S mm?

A

-Adrenergic agents (usually induce contraction)
B2-Adrenergic receptor: coupled to Gs ptn, increases adenylate cyclase, increases cAMP, increases PKA
-Respiratiory: dilation of bronchial S mm open airways
-GI: decrease ,motility of S mm (decrease peristalsis)
Alpha 2 Adrenergic receptor: coupled to Gi ptn, decrease adenylate cyclase, decrese cAMP, decrease PKA
-OPPOSIT OF B2 effects
Alpha 1 Adrenergic receptor: coupled to Gq ptn, PLC-IP3-mediated Ca signaling -CV: peripheral vasoconstriction

  • ACh (Muscaranic receptors: cause most to contract but some to relax)
    • Eye-contraction of the pupil
    • CV-vasodilation of coronary blood vessels
    • Respiratory: constriction of bronchial S mm narrow airways
    • GI: increase motility
    • Renal: contraction of the bladder.
25
Q

What are some hormones, drugs and local metabolites that affect S mm? Study Figure pp 22

A
  • hormones (histamine, serotonin, vasopressin, oxytocin, angiotensin, gastric hormones)
  • Mechanical stretch (opens mechano sensitive channels leading to depolarization)
  • Local metabolites (CO2, lactic acid)
  • Drugs: Ca antagonists, K channel blockers, NO/cGMP stimulators