Section 7: ET - Muscle Flashcards
Skeletal muscle
Voluntary control
Striated
Single long cylindrical cells
Multiple peripheral nuclei
Cardiac muscle
Located only in the heart
Striated
Branched cells with 1-3 (usually 1) central nuclei
Connected via intercalated discs
Involuntary control
Cells much shorter than in skeletal muscle and tend to be zig-zaggy
Smooth muscle
Involuntary
Found in wall of internal organs (gut, blood vessels and iris)
Spindle shaped (fat in middle where nuclei is located), uninucleated cells
Not straited
Structure of skeletal muscle
Attached to bones via tendons
Cells’ muscle fibres are long (up to 35cm) and reasonably wide (0.1mm)
Cells composed of fibrils containing highly organised contractile filaments
Nuclei located under lipid bilayer
Muscle fibre AKA…
Muscle cell
Microscopic structure of myofibrils
Thick filaments: run the entire length of an A band
Thin filaments: run the length of the I band and partway into the A band
Z disc: coin-shaped sheet of proteins than anchor thin filaments and connects myofibrils to each other
H zone: lighter mid-region where filaments don’t overlap
M line: line of protein myomesin that holds adjacent thick filaments together
T-tubules: deep invaginations continuous with the sarcolemma and circle each sarcomere twice at each of the junctions of the A and I bands. Allows APs to be carried deep within muscle cell
Sarcoplasma reticulum (SR): calcium storage site. Terminal cisternae of SR lie close to T-tubules; if AP comes down the T-tubule, it can v quickly signal to SR
Sarcomere extends from … to ……
Extends from one Z disc/line to the next Z disc/line
If Z discs get closer together…
H zone gets smaller and I band gets smaller
A band stays the same length
Myofibril: Thick filaments
Composed of myosin
Each myosin has 2 sub-units each with a globular head and a tail
Many helices joined tgt - all tails joined in middle and heads projected away from M line; polarised
Titin anchors thick filaments to Z line
Myofibril: Thick filaments - head and tail
Head:
An enzyme that hydrolyses ATP (an ATPase)
Have a binding site for actin
Have a hinge that allows them to move
2 tails intertwine to form a helix
Myofibril: Thin filaments
Composed primarily of globular actin proteins
Have a dip in the middle of actin protiens - myosin binding site
Composed of a double-stranded helical actin chain (polymers)
Troponin and tropomyosin
Myofibril: Thin filaments - troponin and tropomyosin
Regulatory proteins associated with actin in skeletal and cardiac muscle
At rest, tropomyosin lies right on top of actin binding sites - stops binding of myosin
Troponin is what calcium binds onto - when Ca2+ binds onto troponin, it changes shape and pulls the tropomyosin off the binding sites
Sliding filament theory of muscle contraction
The sarcomere shortens as the thin filaments are pulled over the thick filaments
Z-line is pulled toward M-line
I band and H zone become narrower
A zone stays the same
Effectively, myosin has stayed still and grabbed onto the actin and pulled it to the middle
Cross bridge cycle - steps (cycle)
- Cross-bridge formation
- activated myosin head binds to actin, forming a cross-bridge
- inorganic phosphate released
- bond between myosin and actin strengthens - Power stroke
- ADP released and activated myosin head rotates (~45° to actin), sliding the thin filament towards centre of sarcomere (M line) –> shortens sarcomere / Z-line by ~9μm
- relaxation phase (where energy is lost) - Cross-bridge detachment
- when another ATP binds to the myosin head, the link between myosin head and actin weakens, and myosin head detaches - Reactivation/energisation of myosin head
- ATP hydrolysed to ADP and inorganic phosphate
- energy released during hydrolysis reactivates myosin head, returning it to the high-energy cocked position (~90° to actin)
Sarcomere
Functional unit of contraction in skeletal muscle fibres
As long as ……. the cross-bridge cycle will repeat
As long as the binding sites on actin remain exposed
As the cross-bridge cycle repeats…
The thin myofilaments are pulled toward each other, and the sarcomere shortens –> causes whole muscle to contract
When does cross-bridge cycle end
When Ca2+ are actively transported back to the SR
Troponin returns to its original shape, allowing tropomyosin to glide over and cover the myosin binding site on actin
Cross-bridges can only occur in presence of…
Calcium, when the myosin binding site on actin is exposed
2 main things happening in the cross-bridge cycle
Mechanical movement
Chemical events
Rigor mortis
When there’s no ATP available, so myosin head is bound onto actin (stiff; doesn’t move)
So, must have ATP to break bond for detachment
Importance of calcium
Provides ‘on’ switch for cross-bridge cycle
When Ca2+ binds with troponin, the tropomyosin moves to expose the myosin binding sites on actin
Cross-bridge cycle will continue as long as Ca2+ levels remain above the critical threshold (0.001-0.01mM)
In high-calcium situations…
There’s muscle contraction
Ca2+ must be free in intracellular space
Skeletal muscle - calcium regulation
Opening of Ca2+ channels in SR allows movement of Ca2+ into cytosol
Active transport pumps (Ca2+ ATPase) are constantly moving Ca2+ from cytoplasm back into SR where it can’t influence troponin
Only when an AP comes along do these channels open and Ca2+ comes out
Isotonic contraction
Shortening (muscles are moving)
Tension constant
Velocity variable
Isometric contraction
No shortening
Length constant
Tension variable
Length-tension relationship - skeletal muscle
During an isometric contraction
At the level of the sarcomere, the max active force (tension developed) is dependent on degree of actin and myosin overlap, i.e. how far its stretched
Active tension - values
At lengths <2.0μm, filaments collide and interfere with each other, reducing force developed At lengths >2.2μm, active forces decline as the extent of overlap between filaments reduces, reducing the no of cross-bridges Maximal force (normal range) between 2.0-2.2μm
If muscle length decreases by half, or more than doubles, it basically becomes useless
Total tension = ?
Active force/tension (dependent on sarcomere length) + passive force/tension
Passive force
As muscle is stretched, the CT around the muscle cells resists the stretch = passive force
Motor unit
Consists of a motor neuron and all the muscle fibres it innervates
Each neuron doesn’t innervate the same one as another - distinct
Excitation-contraction coupling - steps
- ACh released into neuromuscular junction
- an AP travels down motoneuron
- at axon terminal, Ca2+ channels open and Ca2+ enters axon terminal
- triggers vesicles containing ACh to fuse with terminal membrane, releasing ACh into the neuromuscular junction (synaptic cleft) - Activation of ACh receptors
- binding of ACh to receptors on muscle end plate causes opening of ligand (ACh) gated ion channels on post-synaptic membrane
- allows movement of predominantly Na+ into muscle cell making it less -ve (end plate potential) - Muscle AP is triggered
- if sufficient ligand-gated channels are opened, the end plate potential reaches threshold
- voltage-gated Na+ channels open and an AP is triggered
- AP is propagated along sarcolemma into T-tubule system - Calcium is released from SR
- AP is conducted down T-tubules coming in close contact with SR
- results in voltage-gated Ca2+ channels in SR opening (change in shape)
- Ca2+ released into cytosol/sarcoplasm - Ca2+ binds with troponin
- when Ca2+ conc reach a critical threshold, myosin binding sites on actin filament are exposed
6, 7, 8, 9. Cross-bridge cycle - Contraction ends when Ca2+ levels fall
- Ca2+ actively pumped back into SR via Ca2+ ATPase pumps
- troponin moves back to cover myosin binding site
Excitation-contraction coupling: Why are effects of ACh short lasting?
Enzyme acetyl cholinesterase rapidly breaks down ACh
Neuromuscular junction
Site where a motoneuron excites a skeletal muscle
A chemical synapse, consisting of points of contact between axon terminals of a motoneuron and motor end plate of a skeletal muscle fibre
What is excitation-contraction coupling
A sequence of events that converts APs in a muscle fibre to a contraction
Triad
Made up of one portion of a T-tubule and 2 adjacent terminal cisternae
Excitation-contraction coupling: Ca2+ channels
Located in the sarcoplasmic reticulum
Directly linked to voltage-sensor, which is effectively in the sarcolemma / T-tubules
Muscle metabolism: Creatine phosphate
For brief periods (<15s), creatine phosphate can act as an ATP ‘store’ within muscles
Anaerobic
Creatine phosphate + ADP = ?
Creatine + ATP
Anaerobic glycolysis
Good for short intense exercise; fast but inefficient
Dominant system from about 10-30s of maximal effort
Build up of lactate and H+ limits duration to max 120s
Aerobic metabolism
Efficient, but comparatively slow
Requires O2, therefore good blood supply
Max 300W (limits amount of work you can do)
Important for postural muscles and endurance exercise
Source of ATP can be varied, e.g. from fats, amino acids, glucose
Aerobic exercise capacity
As you increase your work rate, you use more O2
Eventually reach a ‘break-point’ (volume of O2 is max)
Muscle fibres - equal?
Not all muscle fibres are equal; type 1 and type 2
Some designed to use aerobic metabolism, and others which primarily use anaerobic metabolism - look different
Muscle fibres - type 1 (slow oxidative)
Max ATPase rate - slow SR pumping capacity - moderate Diameter - small Mitochondria/myoglobin/blood supply - high Glycolytic capacity - moderate Primary ATP pathway - aerobic
Muscle fibres - type 2 (fast glycolytic)
Max ATPase rate - fast
SR pumping capacity - high
Diameter - large
Mitochondria/myoglobin/blood supply - low
Glycolytic capacity - high
Primary ATP pathway - anaerobic glycolysis
Motor units - type 1 (slow twitch)
Units with neurons innervating the slow efficient aerobic cells
e.g. maintaining posture, walking
Type 1 muscle cells referred to as type 1 motor unit
Motor units - type 2 (fast twitch)
Units with neurons innervating the large fibres that fatigue rapidly but develop large forces
e.g. jumping, weight lifting
Type 2 muscle cells referred to as type 2 motor unit
Motor units - type 1 and 2
One motor neuron will come down and only innervate type 1 OR type 2 - not a mix
Regulation of force - dependent on…
Rate of stimulation of individual motor units
Number of motor units recruited
Regulation of force: Rate of stimulation
Single stimulus delivered: muscle contracts and releases - single twitch
If another stimulus is applied before the muscle relaxes completely (low stimulation frequency), more tension results. This is temporal/wave summation and results in unfused/incomplete tetanus
At higher stimulus frequencies, there is no relaxation at all between stimuli - fused (complete) tetanus
Increased frequency of AP = ?
Temporal summation
Skeletal muscle - Twitch vs AP
Twitch lasts longer (multiple times the length) than an AP
Slight delay - twitch starts when AP is done
Tetanus
AKA tetanic contraction
Where twitches merge due to more APs (higher frequency)
Regulation of force: Recruitment
As more units are recruited, tension increases
Usually the most fatigue resistant (small, aerobic) motor units are recruited first, and recruit larger ones last (anaerobic)
Regulation of force: Recruitment - electrical stimulation
Changes voltage on stimulator
The greater the voltage, the more the signal penetrates into the nerve, the more neurons it will get to
Low voltage - below threshold –> none stimulated –> no change in tension
As frequency is increased, more motor units are excited and contraction becomes larger
At highest rate, it’s saturated
Ventricular muscle cells
100μm x 30μm
Lots of mitochondria - heart uses oxidative metabolism
T-tubules are at Z-discs - 1 per sarcomere
Contains intercalated discs - where 2 muscle cells join tgt
Intercalated discs
Desmosomes prevent cells separating during contraction
Gap junctions allow APs to be carried from one cell to the next
Allows for coordinated contraction of all myocytes (unlike skeletal muscle, where fibres are recruited via motor nerves)
Atriums and ventricles
Atriums are receiving chambers
Ventricles have lots of muscle - particularly left ventricle
Cardiac muscle bundles
Figure 8
When heart contracts, it narrows and shortens
Ventricular myocyte AP
AP long lasting >100ms long
Fast depolarisation, but has plateau phase due to presence of large sustained Ca2+ current (I(Ca(L))
MP depolarised throughout most of the ‘twitch’ (heartbeat)
Twitch starts and almost ends before MP comes down to resting level
L-type calcium channel
Voltage-gated channel, but L stands for long (i.e. long time to open and close) –> open for a long time for Ca2+ coming into the cell –> inside of cell stays +ve for a long time –> spread out AP
Cardiac muscle - extended AP
Allows twitch to be almost completed before another AP can come along
While heart is relaxing, blood comes into heart
If no relaxation time, no output from heart because heart doesn’t fill with blood
Cardiac muscle - time spent of heart contracting and relaxing
Usually 1/3 of time contracting and 2/3 of time it is relaxing
Cardiac muscle - exercising AP
When exercising, AP and twitch can get shorter, but still usually 1/3 of time contracting
Cardiac muscle - tetani
Can’t get summation/tetani of twitches - can’t have another beat come along very easily and merge with first one - absolute refractory period
3 major stages of an AP in a cardiac muscle cell
Rapid depolarisation due to fast voltage-gated Na+ channel
Plateau phase due to slow voltage-gated Ca2+ channel (L-type Ca2+ channel)
Repolarisation due to closing of Ca2+ channels and opening of K+ (outward) channels
New AP in cardiac muscle during refractory period
If new AP is triggered during relative refractory period, contraction is quite small
- partly because heart hasn’t been able to fill as much
- would not get a pulse for this contraction because not enough pressure to output aortic blood
May be followed by 2 really quick contractions
Can happen during exercise
Excitation-contraction coupling in ventricular cardiomyocytes - LTCC
L-type voltage-gated calcium channel (I(Ca(L)))
Gets Ca2+ into cell so it combines with troponin
Excitation-contraction coupling in ventricular cardiomyocytes - RyR
Ryanodine receptor (Ca2+ channel in SR) Binds to Ca2+
Excitation-contraction coupling in ventricular cardiomyocytes - NCX
Na+/Ca2+ exchanger
Constantly pumping Ca2+ out of the cell
Excitation-contraction coupling in ventricular cardiomyocytes - NKA
Na+/K+ ATPase
Structural basis for EC-coupling in ventricular cardiomyocytes
SR wrapped around T-tubule
Many channels in T-tubule
Cardiac muscle - excitation-contraction coupling - steps
- Depolarisation opens fast voltage-gated Na+ channels in sarcolemma - reversal of MP from -90mV to +30mV
- Depolarisation wave opens slow LTCC in sarcolemma (DHPR)
- Ca2+ influx balanced by NCX
- Ca2+ influx triggers opening of RyRa in SR –> liberates bursts of Ca2+ (i.e. calcium induce calcium release)
- Raised intracellular Ca2+ conc allows Ca2+ to bind to troponin
- Cross-bridge cycle
Cardiac muscle - for relaxation to occur..
Ca2+ conc inside cell must decline, allowing Ca2+ to dissociate from troponin
Requires Ca2+ transport out of cytosol
Cardiac muscle - methods of Ca2+ transport out of cytosol
SR Ca2+ ATPase
Sarcolemmal NCX
Sarcolemmal Ca2+ ATPase
Mitochondrial Ca2+ uniport
Regulation of Cardiac Ouput (CO) - equation
CO = SV x HR
where CO = cardiac output
SV = stroke volume
HR = heart rate
Heart rate (HR)
Set by pacemaker cells in sinoatrial node
Rate can be modified, especially via autonomic nerves releasing neurotransmitters
Stroke volume (SV)
Reflects tension developed by cardiac muscle fibres in one contraction
Can be increased by:
- increased rate of firing (heart rate) - intrinsic
- increased stretch of ventricles (length) - intrinsic
- certain neurotransmitters (e.g. noradrenaline)
Cardiac output (CO)
Refers to how much blood comes out of the heart in a set period of time
Usually 5 L/min
Cardiac output - exercise
For people who do aerobic exercise, their heart tends to get bigger –> more blood comes out per beat –> heart rate drops to maintain cardiac output of 5L per min at rest
Pacemaker in sinoatrial node determines…
Rate of contraction = heart rate
If MP in SA of heart becomes more -ve, major effect will be a decrease in HR
Sinoatrial node
Specialised muscle cells, where electrical activity in heart initiates, and spreads through the heart
Pacemaker cells (SA + AV node) - pacemaker potential
Slow depolarisation due to I(F) current - mostly Na+ driven
Channels are leaky, so let Na+ into cell –> MP slowly drifts up naturally –> reaches threshold –> AP –> spreads through heart
Pacemaker cells - RMP
Unstable RMP
Depolarisation due to relatively slow Ca2+ current (not fast Na+)
Intrinsic vs resting heart rate
Normally, intrinsic heart rate higher than resting rate because usually at rest, parasympathetic nerve activity is slowing heartrate
Norepinephrine
Noradrenaline
Neural control of heart rate - via alteration of pacemaker potential
Vagal nerves release ACh - decrease rate of spontaneous depolarisation and hyperpolarises RMP –> decrease heart rate
Sympathetic nerves release noradrenaline (NA) - increases rate of spontaneous depolarisation –> increase heart rate
By changing minimum MP…
Can change heart rate
Cardiac muscle - automaticity
Increasing heart rate increases contractile force (stroke volume) –> stronger contractions
Due to less time available for Ca2+ to be pumped out of cell between beats –> tend to start from higher Ca2+ level
Cardiac muscle - troponin saturation
Not all troponin will be saturated, so only some binding sites exposed
If Ca2+ conc increases, more of those binding sites become available
Cardiac muscle - automaticity - the longer between beats…
The more Ca2+ that will go back into the SR
Length tension relationship: Cardiac compared to skeletal muscle
Cardiac muscle is stiffer than skeletal muscle due to stiff components e.g. collagen so it can’t be overstretched –> passive/resting tension becomes more as you stretch it –> total tension is a steeper line for cardiac muscle
Active tension is the same as in skeletal muscle - dependent on actin and myosin overlap
Cardiac muscle - length-tension relationship
More blood put into heart –> gets bigger / more stretched –> more powerful contraction (stroke volume) –> pumps blood out, so heart doesn’t keep getting bigger
Plateaus at 9-10mm of mercury
Entirely intrinsic
Cardiac muscle - length-tension relationship - Starlings law of the heart
As the resting ventricular volume is increased, the force of the contraction is increased
Neural control of stroke volume - noradrenaline
Released by sympathetic nerves leads to increased cytosol Ca2+ due to increased HR shortening time for extrusion, acts on β receptors and via second messengers acts on:
- L-type channels –> Ca2+ influx during AP
- Ca2+ pump in SR so SR increases its Ca2+ stores
Net result = bigger/shorter contraction
Inotropy
Ability of the heart to contract
i.e. contractility
Neural control of stroke volume - increased sympathetic stimulation results in…
Increased output at any filling pressure due to increase in inotropy and heart rate
Smooth muscle - basic structure
Spindle shape, 5μm wide, 100-400μm long with central nuclei
Single unit
Multiunit
Smooth muscle - single unit
Sheets of electrically coupled cells which act in unison, i.e. as one unit - often spontaneously active
Found in most blood vessels and hollow organs
Smooth muscle - multiunit
Tissue made of discrete bundles of independent cells which are densely innervated and contract only in response to its innervation
Each cell is electrically isolated
Arrangement of smooth muscle in walls of hollow organs - unitary smooth muscle
In gut and many blood vessels, tend to have 2 layers of smooth muscle; lying perpendicular to each other
Longitudinal layer - when contracted, they make food move down the gut
Circular layer - when constricted, the narrow it and mush up the food
Smooth muscle - basic cellular structure
No T-tubules - caveolae instead (act to increase SA)
Dense bodies act like Z-lines to anchor actin to sarcolemma
Intermediate filament is cytoskeleton element
Poorly developed SR - volume is much less
Unitary smooth muscle cells
Contain gap junctions which electrically connect the cells together
Smooth muscle - contractile proteins
No striations, but contains actin and myosin filaments Less organised (offset) - allows for greater shortening - can operate over large range of lengths (60-75% shortening possible)
Smooth muscle - initiation of contraction
Electrical behaviour complex but primarily due to voltage-gated Ca2+ channels (relatively few Na+ channels)
Trigger for contraction is an increase in intracellular Ca2+
Ca2+ entering through channels in membrane v important source
Smooth muscle - types of contractions
Neural e.g. arm
Hormonal e.g. uterus
Spontaneous e.g. gut (myogenic - unstable RMP –> fast AP), mostly intrinsic
Source of calcium in smooth muscle
Extracellular (via channels) and SR
Calcium regulation in smooth muscle
Via voltage, hormones, neurotransmitters and specific ions
Ca2+ release in smooth muscle - hormones
Lots of Ca2+ in a cell is released in response to hormones, which trigger receptors through a second messenger pathway, usually involving IP3 which triggers Ca2+ to be released from SR
Smooth muscle: Initiation of contraction - steps
- Ca2+ enters cytosol from ECF via voltage-dependent or independent Ca2+ channels, or from the SR
- Ca2+ binds to and activates calmodulin
- Activated calmodulin activates MLCK
- MLCK activates myosin by phosphorylating it, which activates myosin ATPases
- Activated myosin forms cross-bridges with actin of the thin filaments and shortening begins in the usual fashion
Smooth muscle - calmodulin
In smooth muscle, the regulatory protein is calmodulin and troponin complex is absent
Smooth muscle - MLCK
Myosin light chain kinase
An enzyme
Only active in presence of calmodulin and when it has a Ca bound
Acts on myosin heads
Activation of myosin by MLCK
Regulation is myosin (not actin) based
Myosin doesn’t hydrolyse ATP unless it’s first phosphorylated (on the regulatory light chain, LC20 located on the neck of the myosin)
MLCK phosphorylates the light chain, in the presence of the activated calmodulin
Smooth muscle contractions - speed
Max rate of cross-bridge formation is slow –> slow contractions
Smooth muscle - enzyme regulation
Much slower than channels, so this is a slow (but efficient) process
Conserves energy
Smooth muscle relaxation - when does contraction end
When a MLCP dephosphorylates the myosin light chain
Smooth muscle - MLCP
Myosin light chain phosphatase
Enzyme
Removes phosphate from myosin head - usually result of Ca2+ levels decreasing
Smooth muscle - primary mechanism for reducing intracellular Ca2+
Ca-ATPase in cytoplasm membrane
Smooth muscle - what determines if there’s contraction or relaxation
Balance of the 2 enzymes (kinase of phosphatase)
Increased MLCK activity favours contraction
Increased MLCP activity favours relaxation
When intracellular Ca2+ drops, MLCP activity dominates –> blood flow increases
Smooth muscle: Contraction and relaxation - Ca2+
Ca2+ tends to be the trigger for contraction, not necessarily for relaxation
Smooth muscle - 3 main factors determining modulation of smooth muscle contraction
Cytosol Ca2+
MLCK or
MLCP activity
Changes in any of these will change the tone of the blood vessel
Innervation of smooth muscle
Autonomic nerve fibres branch and form ‘diffuse junctions’ with underlying smooth muscle fibres
Varicosities in the terminal axons contain neurotransmitter, which is secreted into the matrix coating and diffuses to the muscle cells
Smooth muscle - response to stretch
Length-tension relationship similar to skeletal muscle, but when stretched tend to see complex responses
When you stretch smooth muscle, it will generally:
1. Initially contract, effectively resisting the stretch (lots of tension) - stretch activated Ca2+ channels
2. Overtime slowly relax, adapting to change in length - via Ca2+ dependent K+ channels, hyperpolarising the MP
In skeletal muscle, the spread of an AP along the plasma membrane within one myocyte is due to _____, and between adjacent myocytes is dependent on ______
Voltage-gated Na+ channels
Neuronal activation
What factors result in sustained elevated Ca2+ levels in the cytosol?
Reduced ATP availability
Inhibition of acetylcholinesterase
If MP in skeletal muscle cell is at end of repolarisation, tension in muscle cell will most likely be…
Beginning to increase
What is the direct trigger for Ca2+ release from SR in cardiac muscle?
Calcium ions
If a ventricular cardiac myocyte is stimulated at 10Hz for 20s…
The most likely observation is a series of discreet contractions at ~3Hz
Contractions in heart don’t merge, so will get discreet beats
1/3 of time is spent contracting, and 1/3 of 10Hz is approx 3Hz
Which muscle(s) can APs spread from one cell to another
Cardiac, but not skeletal
In ventricles, the most likely combination of AP duration corresponding to contraction is…
AP: 200ms and contraction: 250ms
A drug that blocks Ca2+ ATPase results in…
Greater shortening (decrease in contractility) and slower relaxation of contraction (prolonged contraction) in cardiac cell
If ventricular myocyte is stretched to 1.25x its resting length…
Active tension developed is 25% of optimal
Upregulation of MLCK in vascular smooth muscle results in…
Sustained reduction in radius of blood vessel
Initiation of co-ordinated contraction - skeletal, cardiac and smooth muscle
Dependent on neural activity in skeletal muscle and some smooth muscle, but not cardiac muscle
What happens to total tension if muscle is stretched more than optimal
Becomes more than 100%
In T-tubules of skeletal muscle, ions that contribute to AP are…
Na+ and K+
In skeletal muscle, direct trigger for release of Ca2+ from SR is?
Change in MP
In cardiac muscle, recruitment of muscle cells occur as a consequence of…
Electrical activity spreading from one muscle cell to another
Ventricular myocytes - Na+ current (I(Na))
Essential for directly triggering Ca2+ channels in T-tubules (depolarisation)
Smooth muscle - decrease in intracellular Ca2+ results in…
Reduction in phosphorylation of myosin
If smooth muscle cell is stretched to 1.5x its initial length…
There’s an initial increase in tension, followed by a return to baseline tension over time
Neuromodulator that acts via inward rectifier channels to hyperpolarise vascular smooth muscle cells cause…
A decrease in intracellular Ca2+ and ultimately an increase in blood flow
In the gut, APs are conducted from…
1 smooth muscle cell to another via gap junctions
In a healthy heart, cardiac contraction is triggered by…
Cardiac muscle cells in the SA node
I(F) current (funny current) effect on cells
Spontaneously contracts cell, which contracts at a higher rate than wild-type cells
