MSS- muscle contraction mechanisms Flashcards
outline the roles of muscles
movement - walking, running
hollow organ movement - heart, bv, GI
structure - chambers of the heart etc..
what type of control are muscles under
both voluntary and involuntary
what is the difference between striated and smooth muscle in terms of actin and myosin organisation
smooth - disorganised actin and myosin
skeletal - organised actin and myosin (hence the striations)
how are the skeletal muscles controlled
motor nerves - controlled by the brain
how are smooth muscles controlled
ANS
why is unorganised actin / myosin good for smooth muscle
creates contractions from all dimensions
describe actin
globular protein (G actin) , binds ATP and contains ATPase activity which hydrolyses ATP into ADP and inorganic phosphate
this energy forms chains for G actin to make a helical protein (F actin) which contains active actin binding sites allowing interactions with myosin
describe myosin
2 heavy chains, 4 light chains, 2 heavy chains are intertwined producing N terminal head domains which bind to actin
these head domains bind ATP and ADP and contain ATPase activity
where is tropomyosin found
striated muscle
what is the function of tropomyosin
wraps around acting which covers the active actin binding sites at rest
this means that actin and myosin wont come together at rest
troponin system - TnI, TnC, TnT
how is muscle contraction initiated
rise in Ca inside muscle cells
increase in calcium leads to the removal of tropomyosin from the actin binding sites
therefore exposed sites are able to attach to myosin
how is a rise in calcium produced
extracellular concentration of Ca - 1-2 mM
intracellular concentration of Ca - 100nM
calcium stored in SR and diffusion from outside the cells increases Ca in cytoplasm removing tropomyosin
describe the action of myosin during contraction
ATP binds to myosin heavy chain heads - low affinity for actin binding
hydrolysis of ATP at myosin heads means they become energised and oriented - high affinity for actin binding sites
interaction between actin and myosin releases a phosphate molecule which allows binding
the myosin binds to the actin forming cross bridges
outline the sliding filament hypothesis
after myosin / acting binding
90degree cocking motion where ADP is released - more energy to reaction
a 45 degree cocking motion is then produced between actin and myosin
acts like a rowing motions - causes a shortening between the sarcomeres
myosin cross bridges rotate towards the centre of the sarcomere - power stroke
as ADP is now absent the myosin comes away from the actin binding site - allowing the cycle to start again
what is rigor mortis
a consequence of the sliding filament hypothesis
myosin heads need to be constantly primed with ATP to be ready for contraction
what is the process behind rigor mortis
needs ATP for myosin binding and for detachment of myosin - actin
in death:
increase in calcium = removal of tropomyosin from actin
loss of ATP production prevents detachment of actin - myosin filaments - causes the stiffness of muscles
starts 2-6 hours after death - peaks at 12 hours)
stops at 24-48 hours due to decomposition of myosin / actin proteins
explain how a rise of calcium allows the uncovering of actin binding sites by tropomyosin
TnT - binds to tropomyosin
TnI- binds to actin sites
TnC- binds to calcium
calcium binds to TnC
causing a conformational change of the TnT/TnI tropomyosin complex
leads to the exposure of actin active sites allowing the myosin to bind and the initiation of the sliding filament hypothesis
describe the activation of nicotinic ligand gated receptors in skeletal muscle
activation by Ach (released by motor nerves)
Ach binds to alpha subunit of ligand receptors - allows sodium into the cell
how are nicotinic receptors activated at the NMJ
conduction of action potential in the motor nerves
causes voltage gated calcium channels to open causing calcium influx and the formation of Ach vesicles
these vesicles (due to calcium) bind the the cleft and release into the synapse
move along the concentration gradient and bind to alpha subunit of the nicotinic receptor
this activation brings sodium into the skeletal cell
the influx of sodium causes depolarisation which activated the voltage gated calcium channels - contraction
breakdown of Ach by AchE = termination of response - choline recycled into the neurone and acetyl CoA is washed out
how is skeletal muscle contracted
action potential is conducted through skeletal muscle via t-tubules
the action potential opens voltage gated calcium channels with have a direct connection with the ryr of the SR
ryr allows stored calcium to go into the cytoplasm where it increases calcium level and allows binding of actin and myosin
outline how stimulation of beta 1 adrenoreceptors increases contractility of cardiac muscle
electrical activity generated in SAN
action potential stimulates the opening of VGCC which allows calcium into the cell
not directly linked with the SR
calcium induced calcium release
triggers contraction
activation of beta 1 adrenoreceptors
(gs)
stimulation converted ATP to cAMP (intracellular messenger)
cAMP production triggers PKA, whcih phosphorylates VGCC and ryr receptors
causes more VGCC to open = increase in Ca influx
PKA stimulates ryr receptor = calcium release
= increased contraction
how do you produce relaxation in muscle
lower Ca inside the cell using CAATPase and using sodium exchanger
CAATPase transport calcium into storage - against concentration gradient
a decrease in Ca causes a reduced TNC Ca binding, therefore leading to tropomyosin to bind back onto actin binding sites - preventing interaction
where is smooth muscle found
walls of tubular organs - blood vessels, GI tract, airways, uterus, bladder, eye
what are the characteristics of smooth muscle contraction
slow, sustained, graded relative weak innervated by ANS can have myogenic contractions excitable cells produce action potentials like skeletal muscle and cariad muscle
