19. Smooth M. Phys Flashcards by Priyanka Barad

How do skeletal M and smooth M vary in regards to histology

Sk. M - large, multinucleated, striate cells
Sm. M- small, single nucleus w no striations

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How do skeletal M and smooth M vary in regards to the SR

Sk M - large well developed; SR w/ triad well developed T-tubules
Sm M - poorly developed SR & t-tubules; membrane contain calveolae

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How do skeletal M and smooth M vary in regards to thin filaments

-Sk. M - actin, tropomyosin, troponin (less thin filaments than Sm. M)

Sm. M - actin, tropomyosin & CALMODULIN

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How do skeletal M and smooth M vary in regards to thick filaments

-Sk. M - myosin, ATPase activity = faster (more in number than Sm. M) -

Sm. M - myosin, ATPase activity slower, myosin light chains prominent

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How do skeletal M and smooth M vary in regards to innervation

Sk. M - alpha- MN
Sm. M - multiple types (intrinsic & ANS)

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How do skeletal M and smooth M vary in regards to NTs

Sk. M - Ach - excitatory
Sm. M - Ach (inhibitory) & NE/Epi (excitatory)

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How do skeletal M and smooth M vary in regards to transmission specialization

Sk. M - NMJ
Sm. M - varicosities

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How do skeletal M and smooth M vary in regards to NT receptors

Sk. M - nAChR
Sm. M - mAChR, adrenergic, etc

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How do skeletal M and smooth M vary in regards to other forms of activation

Sk. M - none
Sm. M - blood-borne, paracrine, intrinsic

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How do skeletal M and smooth M vary in regards to AP

Sk. M - required
Sm. M - not required! - pace maker activity

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How do skeletal M and smooth M vary in regards to source of Ca

Sk. M - release from SR
Sm. M - mostly from ECF influx & some from SR

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How do skeletal M and smooth M vary in regards to role of Ca

Sk. M - bind troponin C
Sm. M - bind calmodulin —> activate MLCK

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How do skeletal M and smooth M vary in regards to how actin and myosin bind

Sk. M - tropomyosin moved by troponin
Sm. M - phosphorylate myosin light chain via kinase

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How do skeletal M and smooth M vary in regards to relaxation

Sk. M - remove Ca from troponin
Sm. M - activate light chain PHOSPHATASE - dephos —> inactivate

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What does it mean to be a multi-unit Sm M

fibers operate individually, innervated by single N with multiple varicosities
for fine tuning

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What is a unitary Sm M

Where are they located

visceral Sm M or syncytial
work together as a unit
cell mems adhere & contain gap jxns
in GI (help move food), bile duct, uterus

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What are the ways Sm M can be arranged

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-circumferential -

circumferential & longitudinal

-varied

Where does actin bind in Sm M & why is it special

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attach to dense bodies & adheres jxns
dense bodies can rearrange fibers to help w/ length-tension relationship

What is the arrangement of myosin in Sm. M

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-bi-directional

How is myosin cross-bridge cycling diff in Sm. M

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slower!
myosin & actin attached longer —> greater force
less ATP needed

How can Ca increase in the cytosol (aka stimulate Sm. M)

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N innervation
hormone
stretch
environmental cues

What are IP3-gated Ca channels

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-once some Ca into the cell, they can bind these channels and allow a little more Ca release from SR

What are the ways Ca can enter the cell

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-NT binds and activate Ca channel in sarcolemma—> Ca in
-in the cell Ca can activate Vg Ca (L-type Ca channels) in sarcolemma —> Ca in
-ryansidine receptors on SR —> Ca out of SR
-IP3 receptors —> activated by hormones/NTs on cell surface —> IP3 - 2nd messenger —> bind on SR —> increase Ca out of SR

How can Ca exit the cell

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SERCA (back into SR)
3Na/Ca anti porter - Ca out of cell by trading Na
sarcolemmal Ca ATPase

What happens when Ca binds calmodulin (CaM)

- 4 Ca ions bind CaM -change conformation —\> activate - activate MLCK —\> phos myosin - allow myosin to bind actin —\> contraction

How does SM M relaxation occur

- Ca pump to remove Ca - & myosin light chain PHOSPHATASE —\> dephos myosin light chain _-need both for full relaxation_

What are varicosities

- NT release sites - distance btn varicosities and fibers differ

What is the response generated by NE/Epi

-varies by receptor - alpha 1- contract - beta 2- relax

How do Sm Ms respond to Ach

- varies depending on organ - contraction = direct effect - relaxation = indirect effect

What does angiotensin II, vasopressin & endothelin do

contract Sm M

What is the effect of adenosine

-relax Sm M

How doe Sm M respond to NO

NO = inhibitory —\> Sm M relaxes

What are some environmental cues that Sm M will respond to?

-hypoxia -excess CO2 -increased H+ - adenosine, LA, increased K+

What environmental cues will lead to vasodilation

- decrease O2 or sym tone - increase Co2, H+ or K+ -prostaglandins, adenosine, NO, ANP

What environmental cues will lead to vasoconstriction

- stretch - endothelins - increase sym tone - angiotensin II, ADH, NE, Epi

What is the latch mechanism

- generate some force for a given amount of Ca - allow binding w slow to fatigue myosin ATPase \*ATP still present, myosin head still phos bc still have some Ca —\> keep cycling (slowly) but w/ less ATP! -increase tension w/ little ATP

What is RMP for Sm M

-50 to -60

What two forms of Sm M activity do you have

- plateaus - spike potentials

describe general Sm M activity

- slow wave oscillations via Ca influx (L type Vg Ca) & K efflux (Ca activated K channels) - spike potentials occur w/ stimulation of hormone, NT, stretch, spontaneous - plateaus occur w/ stimulation of NT and stretch

Compare and contrast length-tension relationship ban Sk. M and Sm. M

-both - get stretched —\> increase force -Sm M- rearrange fibers to get greater stretch & shift L/R for optimal range

19. Smooth M. Phys Flashcards

(40 cards)