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smooth muscle: general features
lack visible cross-striations - actin and myosin filaments not as regularly arranged
long, spindle-shaped cells with single nucleus
cells usually arranged in sheets within muscle
no z lines - dense bodies instead
less mitochondria and more poorly developed sarcoplasmic reticulum
no troponin, tropomyosin doesn’t block cross-bridge binding sites
smooth muscle: organisation of thin and thick filaments
actin and myosin filaments at slight diagonal from side to side - diamond shaped lattice
myosin molecules arranged in thick filaments so cross-bridges present across entire length - allows thin filaments to be pulled along the thick filaments
intermediate filaments part of cytoskeletal framework supporting cells shape
dense bodies contain same proteins as z lines
smooth muscle: contraction
Ca2+ ions bind to calmodulin to form a complex
Ca2+-calmodulin complex activates myosin kinase
myosin kinase phosphorylates myosin heads using ATP hydrolysis
phosphorylated myosin can interact with actin filaments to form actin-myosin crossbridges so contraction can take place
when Ca2+ ions removed from sarcoplasm they dissociate from calmodulin so myosin kinase activity falls
myosin is dephosphorylated by myosin phosphatase
but Ca2+ ion removal is slower so contraction is longer and gives a more graded response
smooth muscle: different types
multi-unit smooth muscle:
neurogenic - stimulated by nerves
made from multiple discrete units which function independently - no gap junctions
units must be separately stimulated by nerves to contract
single-unit smooth muscle:
myogenic - no nervous stimulation required for contraction
fibres excited and contract as a unit - gap junctions present so AP generated in one smooth muscle cell spreads to all cells in that
slow and energy efficient contraction
functional syncytium - contract as one
smooth muscle: single-unit contraction
can be phasic or tonic
phasic - contracts in bursts, triggered by action potential which leads to increase in cystolic Ca2+
tonic - often partially contracted at all times, doesn’t show burst of activity like phasic but varies in increments above or below usual tonic state
smooth muscle: factors affecting contractile activity
spontaneous depolarisation of cells
signaling molecules:
neurotransmitters from autonomic neurons - neurotransmitters of (para)sympathetic postganglionic cells alter membrane potential of smooth muscle cells to make them more/less likely to fire APs and contract
hormones
local changes in extracellular fluid
stretch:
vascular smooth muscle cells respond to stretch by contracting - membranes of stretched cells depolarise and fire APs, causing cells to contract
smooth muscle can continue to develop tension even when very stretched - stress relaxation response
cardiac output
stroke volume x heart rate
cardiac muscle: general features
found in walls of heart
regular arrangements of actin and myosin filaments - striations
Z lines present
cells joined at intercalated discs - provide strong mechanical adhesions between adjacent cells so muscle can withstand high pressures when pumping blood
Gap junctions between cells - syncytium, AP initiated at one point in cardiac muscle spreads so that a large number of cardiac cells contract simultaneously
T-tubule system present
innervated by autonomic nervous system
cardiac muscle: generation of AP
resting membrane potential - approx - 90mv
heartbeat autorhythmic - generated by heart muscle
AP generated by pacemaker cells
pacemaker cells have low density of actin and myosin filaments, initiate and coordinate rhythmic contractions of heart
Each AP triggers full contraction followed by relaxation
cardiac muscle: T tubule system
T tubules larger
have DHP voltage gated ion channels which open to allow Ca2+ ions into sarcoplasm - Ca2+ ions bind to ryanodine receptors so more Ca2+ ion channels opened which leads to fibre contraction
this is known as Ca2+- induced Ca2+ release
cardiac muscle: action potentials
spontaneous, rapid depolarisation of cells occurs
plateau phase - slow as Ca2+ ions move in slowly
slow repolarisation
rhythmic firing
SA and AV nodes pacemaker cells - result in certain firing rate with vagus nerves
Firing rate controlled by sympathetic and parasympathetic nervous systems - modifies rate at which pacemaker cells fire
latent pacemakers located in conduction system - keeps heart beating if other pacemakers fail
cardiac muscle: firing of pacemaker cells
movement of Na+, K+ and Ca2+ via ion channels
at -60mv, Na+ ion channels open - slow inward current
slow depolarisation as Ca2+ ion channels open
K+ ion channels open to cause repolarization, when closed followed by slow depolarisation again
long refractory period prevents summation (tetanus) - second AP can’t be generated until excitable membrane has recovered from first