muscle 2 Flashcards
how does smooth muscle differ from cardiac and skeletal muscle
-lacks striated pattern
-contains sense bodies throughout cytoplasm and plasma membrane. analogous to Z lines in skeletal muscle
-dense bodies, actin, myosin network connects to cytoskeletal network of non- contracting intermediate dilaments- house frame- that connects to plasma membrane
-contracts via sliding filament mechanism like cardiac and skeletal muscle
what innervates smooth muscle
sympathetic and parasympathetic nerves
autonomic nerves and smooth muscle
acon divides into multiple acons to form fish net like plexus that surrounds SM
what do the axons of the plexus form
structures called varicosities which are the sites of transmitter release
multiple varicosities along each axon. one AP stimulates many varicosities like a sprinkler system
varicosities and junctions
dont form distinct motor junctions like. smooth muscle cell can recieve transmitters from multiple varicosities including varicosities from sympathetic and parasympathetic nerves
what causes contraction
elevation in Ca
what augments contraction
enhancement of actin/ myosin cross bridging
SM and relaxing mechanisms
has unique mechanisms that inhibit cross bridging
the type of response (contraction vs relaxation) within a smooth muscle depends on
-type and predominance of ANS innervation. symp vs. parasymp
-predominance and subtype of receptor which is being stimulated by acetylcholine or noradrenaline
Ability of transmitter to access a given receptor
a1
contract SM
predominantly via pharmacomechanical contraction through SR ca release and PKC activation
b2
relax SM via pharmacomechanical relaxation by increasing intracellular CAMP
M2 +M3
increase pacemaker cell activity in the gut, enhancing gut contraction and peristaltic movement via electromechanical coupling
M3
contract SM via pharmacomechanical contraction through SR Ca release and PKC activation like a1 receptors
what activates muscranic receptors
acetylcholine released by parasympathetic nerves
what receptors most often contract SM
muscranic receptors
what do muscranic receptors do in the blood cessels
act on endothelium to produce SM relaxation
what do M3 receptors do in the endothelium of blood vessels
either release NO and or produce the transmission of hyperpolarization to the SM via gap junctions between the endothelium and SM . both mechanisms relax SM
pharmacomechanical coupling
contraction or relaxation not mediated by a change in SM cell membrane potential
produced via a biochemical event within SM cell with no movement of ions across membrane
cell membrane potential does not alter during contraction or relaxation
electromechanical coupling
contraction or relaxation mediated by a change in SM membrane potential. produced by opening of Ca channel (L type Ca channel) in response to depolarization- contraction- or closing of the same channel in response to hyperpolarization- relaxation-
skeletal and cardiac muscle contraction
soley mediated via electromechanical coupling- AP formation
pheamomechanical contraction is produced through
intracellular release of Ca from sarcoplasmic reticiulum via IP3 receptors and/or activation of protein kinase C which enhances myosin actin cross bridging. in many cases this mechanism combines with electromechanical contraction
every smooth muscle can contract using this mechanism
intracellular release of Ca from sarcoplasmic reticiulum via IP3 receptors and/or activation of protein kinase C which enhances myosin actin cross bridging. in many cases this mechanism combines with electromechanical contraction
pharmacomechanical relaxation
virtually always produced by an intracellular elevation in CAMP of CGMP which respectively activates CAMP OR CGMP dependant protein kinases that inhibit myosin/actin cross bridging
what is electromechanical contraction mediated by
SM membrane depolarization
what is electromechanical relazation mediated by
SM membrane hyperpolarization
what does SM membrane depolarization lead to
opens voltage gated ca channels in all SM in in some it initiates Ca ac tion potentials via the same gated ca channel. this promotes contraction
what does SM hyperpolarization lead to
the closing of ca channels and inhibition of ca APs and this leads to relxation
how do SM cells increase intracellular Ca
- generation AP which are produced by ca not na influx in SM
- depolarization but no AP
both mediated by L type ca channel
what causes electromechanical coupling and pharmacomechanical coupling to occur together
sympathetic or parasympathetic nerve stimulation via ATP co release with noradrenaline or acetylcholine
what produces excitatory junction potentials
sympathetic or parasympathetic nerve stimultaion in some SM tissue
what can ejps do if they are large enough
eleicit ca APs
what produces ejps
the co release of ATP from the nerves
multiunit SM cells
not electrically connected with gap junctions
depo or hyperpolarization can no spread from cell to cell via gap junction
system similar to skeletal muscle- individual contraction
unitary SM cells
are electrically connected with gap junctions
cell depolarization can spread via gap junction bw cells
system similar to cardiac muscle
what must unitary cells exhibit
electromechanical coupling bc they have to be able to depolarize and hyperpolarize
what do parasyptathetic nerves and acetylcholine increase
slow wave frequency, peristalsis and SMC contraction via M3 receptors
what do sympathetic nerves and noradrenaline lead to
reduction of SW frequency, peristalsis and relax the SMC via B receptors
setup of stomach and intestines
composed of SMC that are connected with gap junctions that allow transmission of depolarization from cell to cell
what is imbedded bw the SMC in the stomach and intestines
non SMC pacemaker cells that produce slow waves of depolarization that are transmitted to the SMC which intiate ca AP fomratio within the SMC causing coordinated phasic contraction resultnig in peristalsis that moves food through the gut
ELECTROMECHANICALLY COUPLED SYSTEM
example of non SMC cells
intersitital cells of cajal
does SM have toponin
no
what does ca bind to in SM
molecule called calmodulin fomring complex that activates an enxyme MLCK
what si MLCK
myosin light chain kinase
what does MLCK do
phosphorylates myosin which activates myosin ATPase activity which initiates myosin cross-bridging with actin to produce contraction
sacromere structure in cardiac muscle compared to skeletal muscle
organiation of all the parts is similar
mechanism of contraction in heart vs skseletal muscle
identical
what is the difference between heart and skeletal muscle
- heart is spontaneously active. no direct motor nerve connection to CNS
contraction initiated and maintained by rhythmically by intrinsic pacemaker cells producing action potentials within SA node - AP transmitted bw cells thru gap junctions within intercalated discs forming tunnels bw cells
volume fraction of mitochondria of heart compared to skeletal
20x
capilary density of cardiac vs skeletal muscle
7.5x
o2 extraction heart vs skeletal
more o2 extraction
myoglobin content of heart vs skeletal
high in heart
phosphorylation method of heart vs skeletal
almost exclusively oxidative phosphorylation in heart as opposed to glycolysis
heart muscle twitch characteristic resemblence
fast twitch but its characteristics are of the slow twitch muscle
sequential contraction of atria
a- atria and ventricles fill when heart is relaxed
b- atrai contract forcing more blood into centricles
c- after a delay, ventricles contract simultaneously pushing bood into lungs and body
what forms a conduction system
modified cardiac cells
where does the conduction system start and propagate to
in the SA node and propagates AP to the atrai then to the venticles initiating contrcation in the cardiac muscle cell within both areas
what is the hearts pacemaker
the sa node
what does the sa node produce
spontaneous repetitive unique ca not na driven AP
AP process of SA node
- resting at -60 mv and leaky to na and ca and influx of both slowly depolarizes the cell
- at threshold of -40mv ap is produced via a fast influx of ca and platueaus at 0mv
- depolarization to 0 triggers a rapid efflu of k which hyperpolarizes the cell back to -60mv
repeat about 70 times per min which is average heart rate in humans
what are gap junctions
protein tunnesl that connnect cytoplasm of adjacent cells and transmits depolarization
where do AP in the SA node spread to
spread thru conduction system and depolarize atrial and ventricular cardiac muscle cells causing them to evoke AP and contract
what can every cardiac cell do when it is depolarized ot threshold
evoke a AP
what is a fact about the cell siwthin the conducting system
cant contract byt they transmit depolarixationt othe cells in the atria and vetricles which can contract
difference bw ca driven AP in sa node and atrial and ventricullar cells
atrial and ventricular cells are driven by na influx which leads to depolarization which leads to ca influx thru special voltage gated channels
ca small influx is important bc it triggers large release of ca from the sarcoplasmic reticulum resulting in contraction
sequence of depolarization and subsequent contraction in the heart
- SA node spontaneously fires AP and depolarization spreads through the atria producing APs in the atrial muscle cells
- atrial contraction results pushing blood into ventricles
- 0.13 delay and then depolarization and AP transmitted down conducting system to the apex of the ventricle
- depol and AP sread from apex/ bottom up thru the ventricle cells producing contraction and squeezing blood into lungs and body
AP travelling in skeletal muscle
travels thru T tubule system and activates DHP receptor which mechanically releases ca from sarcoplasmic reticulum
cardiac muscle AP travelling
thru plasma membrane and T tubule system and opens voltage gated ca channels and ca enters inducing release of ca from sarcoplasmic reticulum
what controls heart rate and strength of ventricular contraction
PNS AND SNS
SNS and heart rate and strength of ventricular contraction
releases noradrenaline and adrenaline from adrenal gland- bind to B1 receptor- depolarizes SA- inc heart rate- enhance ca release- inc force of contraction- more blood from ventricles
another name for PNS
vagal
PNS heart rate and strength of ventricular contraction
releases acetylcholine which binds to muscranic M2 receptors- hyperpolarization of SA and conducting system- reduces SA node fiding and slowing heart rate
what happens when heart ventircles fill with blood
cardiac cells stretch
what does stretching of cardiac cells and skeletal muscle produce
more optimal orientation of actin and myosin allowing greater contrcatile force to be generated
whta does more blood pushed into heart lead to
greater contractility of heart cells and larger ejection fraction of blood pumped out of heart named STARLINGS LAW OF THE HEART
