Skeletal Smooth And Cardiac Muscle Comparison Summary Flashcards
Describe the Skeletal muscle?
Striated
It’s mechanism of exitiation is by neuromuscular transmission
Electrical activity off muscle cell- action potential spikes
It’s calcium sensor is TROPONIN C
Cross ridge reaction occurs
Excitation-contraction coupling- L- type ca Channels- DHP RECEPTORS) in t tubule membrane coupling to ca released channel |( RYANODINE) RECEPTOR in SR
Terminates contraction by breakdown of ach ach esterase
Metabolism ,mechanism- oxidative, glycolytic
Type 1, 11a, 11x
Fastest 5-10s
Short term high intensity - creating phosphate
Describe smooth muscle ?
Lacks striations- as thick and thin filaments are not organised in sacromeres
Found in walls of hollow organs - gi tract- bladder- uterus
2 major categories- multi and single nucleate
Has gap junctions between cells- allows for fast spread of electrical activity- low resistance flow (urinary sm)
Combi of both is found in - vascular smooth muscle
No troponin- ca2 binds to calmodulin in stead . Which regulates myosin light chain kinase- which regulates cross bridging
Mechanism of excitation - synaptic transmission, hormone activated receptors, electron coupling, pacemaker potentials.
Ca2 entry through - Ip3 ,dhp, voltage gated, calcium induced release from sr. And through ca store operated channels
Electrical activity of muscle - action p strikes, slow waves, graded mp
Oxidative
Mlck dephosphorylates through proteases
Glycolysis’ (anaerobic) Less fast
High intensity exercises- lacid
Describe cardiac muscle ?
Striated
Mechanism of action- pacemaker potentials, electronic deposit through gap junctions
EA OF MUSCLE CELLS- AP PLATEAUS
TROPONIN ca2 sensor
Ec coupling- ca2 en try through l type ca channel( dhp receptor)
Triggers ca2 induced ca release from sr
Terminates contraction by ap repolerisation
Oxidative.
Ca-na and na-k pump
Krebs-slow- endurance exercise- long term
Define iontropism
Is the insintric ability oof myocardial cells to develop force at a given muscle cell length.
Agents that produce increase in contractility - positive- increases rate of tension develop and peak tension.
What is parasympathetic nervous system?
Whereby stimulation of psn and ACH have negative ion0tropic affect on atria.
This effect is mediated by Muscarinic receptors - coupled via gk protein to ADENYL Cyclase
G protein is inhibitory- decreases contractility
Sympathetic Nervous System
Stimulation of sns and circulations CHOLAMINES have positive ions tropic affect
On myocardium.
Which increases perks tension. Increased rate of tension and faster rate of relaxation.
Faster relaxation= contraction= shorter= allows more time for refilling
Mediated by B receptors coupled via d protein ton adenyl cylase
Ac activation leads to production of adenosine mono phosphate, protein kinases, phoshorylation of proteins
That produce effect of increased contractility
PHOSHPHOLAMBAN- protein that regulates ca atpase in sr
Positive staircase affect
Bodwitch staircase or Treppe
When heart rate doubles- tension developed on each beat increases in stepwise fashion to maximal value.
Increase in tension due to increase ap per unit time.
Very first heart beat- non increase in tension as ca2 has not yet accumulated.
With each beat ca2 is accumulated by sr until storage level is maximum
Postextrasystolic Potentiation
When an extra systole occurs- anomaly- extra beat generated by latent pace maker
Tension developed on next beat is greater than normal- unexpected or extra ca enters cell during extrasystole and was accumulated by sr
Where is multi unit smooth muscle found
In the iris, ciliary muscles of lens and in vas deferens
Each fiber behaves as separate motor unit- little to no coupling between cells
Multi unit sm cells are densely innervate by postganglionic fibres of para and sympathetic ns
Which regulate function
Describe depolarisation of sm
1- depolarisation of sm- opens voltage gated ca channels in sarcolemal membrabe
Ca flows into cell down ecg.
Influx from ecf causes increase in intracellular ca con
Subthreshold depolarisation can open these channels
If depo reaches threshold then ap can occur causing even greater depo and even greater opening of ca channels
Ca entering sm cells through vgc causes ca induced ca release from sr
What are the other two ways in which ca conc can accumulate in cells
1- ca can enter through ligand gated ca channels in sacrollemal membrane- which can be opened by hormones/ neurotransmitters and permit entry of additional ca from ecf
2- inositol - ip3- gated channels- in membrane of sr can also be opened by neurotransmitters/hormones
Next step
Rise in IC ca con causes ca to bind to calmodulin
Which like tc binds 4 ions of ca
Ca-calmodulin complex binds to + activates myosin light chain kinase
Which when activated phosphorylase’s myosin light chain- which in turn causes conformational change in head of myosin- which greatly increases atpase activity- which allows myosin to bind to actin
Thus initiating cross bridge cycling and production of tension.
Amount of tension is proportional to IC CA CONC
What other affects does ca- calmodulin Complex have
Has 2 affects on two filament proteins- caplonin, caldesmon
At low levels of ic of ca both of these bind actin- inhibiting myosin atpase+ interaction of m/a
When ic ca increases ca-calmodulin complex phosphorylase’s calponin/caldesmon-releasingtheir inhibition
Myosin atpase- facilitating formation of cb between m/a
Describe relaxation of sm
Occurs when ic ca con falls below level needed to form ca-calmodulin complex
Fall can occur by many mechanisms: hyperpolerisation - closing volt-gat-ca channels
Direct inhibition of ca channels by ligands such as cyclic camp/gmp
Inhibition of ip3 production
Decreased release of ca from sr
Increased ca atpase activity in sr-
Relaxation of sm cab involve activation of Mlc phosphatase- dephosphorylates mlc- leading to inhibition of myosin atpase
Ca - desensitisation
