19. Smooth M. Phys Flashcards
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
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
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
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
How do skeletal M and smooth M vary in regards to innervation
- Sk. M - alpha- MN
- Sm. M - multiple types (intrinsic & ANS)
How do skeletal M and smooth M vary in regards to NTs
- Sk. M - Ach - excitatory
- Sm. M - Ach (inhibitory) & NE/Epi (excitatory)
How do skeletal M and smooth M vary in regards to transmission specialization
- Sk. M - NMJ
- Sm. M - varicosities
How do skeletal M and smooth M vary in regards to NT receptors
- Sk. M - nAChR
- Sm. M - mAChR, adrenergic, etc
How do skeletal M and smooth M vary in regards to other forms of activation
- Sk. M - none
- Sm. M - blood-borne, paracrine, intrinsic
How do skeletal M and smooth M vary in regards to AP
- Sk. M - required
- Sm. M - not required! - pace maker activity
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
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
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
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
What does it mean to be a multi-unit Sm M
- fibers operate individually, innervated by single N with multiple varicosities
- for fine tuning
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
What are the ways Sm M can be arranged
-circumferential -
circumferential & longitudinal
-varied
Where does actin bind in Sm M & why is it special
- 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
-bi-directional
How is myosin cross-bridge cycling diff in Sm. M
- slower!
- myosin & actin attached longer —> greater force
- less ATP needed
How can Ca increase in the cytosol (aka stimulate Sm. M)
- N innervation
- hormone
- stretch
- environmental cues
What are IP3-gated Ca channels
-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
- -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
- 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
