What is this muscle?
What is this muscle?
What is this muscle?
What are the characteristics of
a) skeletal muscle
b) cardiac muscle
c) smooth muscle
a) striated, multinuclear and peripheral, for locomotion, sarcomeres, Ca2+ binding=troponin
b) striated, meshwork, central nucleus, intrinsic myogenic activity, sarcomeres, Ca2+ binding=troponin
c) involuntary, non-striated, 1 nucleus per fibre, spindle shape, mechanical organ control, no sarcomeres, Ca2+=calmodulin
Do skeletal, cardiac and smooth have cellular junctions?
skeletal - none
cardiac - intercalated discs, gap junctions
smooth - gap junctions
What is an intercalated disc and where are they found?
Thickenning of sarcolemma, connects adjoining cardiac myocetes e.g desmosomes and gap junctions. Found in cardiac muscle only
A: gap junction
B: intercalated disc
C: sarcoplasmic reticulum
D: A band (thick)
E: I band (thin)
F: Z disc
Cardiac cells have automaticity and rhythmicity - what does this mean?
Can spontaneously generate electrical impulses (depolarise) in a regular and repetitive manner
(pacemaker cells in SAN and AVN)
Cardiac myocetes from an electical/functional syncytium - what does this mean?
Electrical impulses propagate between cells via gap junctions on intercalated discs, waves of depol. propagate to adjacent cells which contract in a synchronous fashion
NB: diff size/shape of APs in heart and many ion channels involved in response. Na+ Ca2+ depol, and K+ repol
What two types of cells are found in the heart?
Pacemaker cells (SAN, AVN, have automacity)
Ventricular cells (have refractory periods)
Describe the process of Ca2+ signalling during cardiac contraction.
1. Na+ in, membrane depolarises, VGCa2+ channels open (L type)
2. Ca2+ influx, intracellular Ca2+ increases triggering Ca2+ release from sarcoplasmic reticulum
3. Ca2+ associates with troponin C in sarcomere and stimulates contraction (systole) (unmasks binding site for M to bind with A)
4. Ca2+ released from sarcomere causes diastole and its reuptake into sarcoplasmic reticulum
NB: ATP hydrolosis provides energy to drive filament sliding
What happens to the heart under sympathetic and parasympathetic modulation?
Sympathetic: increased heart rate and contraction force, NA secretion and activation of beta1 adrenoreceptor
Parasympathetic: decreased heart rate, ACh secretion and activation of muscarinic receptors (M2)
What is this structure?
A: intermediate filament
B: dense body
C: mechanical junction coupling cells
D: gap junction for electrical and chemical communication
Describe smooth muscle.
What do intermediate filaments do?
What do dense bodies do?
What are the 2 types of attachments between cells?
Loose lattice of thick and thin filaments running obliquely across muscle.
Assist in transmission of contraction force
Attachements for thick and thin filaments
Mechanical and gap junctions (electical signals)
List the structures where smooth muscle is found
- Gut (oseophagus, stomach, intestines) (propel food through GI tract)
- Uterus (deliver baby)
BVs (regulate BV diameter)
Bronchi (regulate airway diameter)
- Urethra, bladder
- Errector pili in skin
What innervates smooth muscle?
Where do nerves make multiple contacts with a smooth muscle cell? Describe the process.
What are the 2 forms of contraction initiation in smooth muscle?
Varicosities. They release NT into space surrounding muscle, NT receptors widely spread across postsynaptic membrane.
1. gap junction connections 2. neuronal innervation (ANS)
What are the 2 types of smooth muscle organisation?
What are the differences?
1. multiunit SM 2. single unit SM
Multiunit SM: each cell receives synaptic input and contracts independantly, LITTLE ELECTRICAL COUPLING. For fine control and gradual responses e.g. intrinsic eye muscles, large BVs
Singleunit SM: ANS innervates 1 cell within sheet/bundle, AP propagated by gap junctions, WHOLE BUNDLE/SHEET CONTRACATS as functional syncytium. For slow, steady contractions e.g. visceral oragns - GI tract
What types of cells are A and B?
A: Multiunit SM cell
B: Single unit SM cell
Compare SM action potential generation to skeletal
AP in SM longer (10-50ms) than skkeletal (2ms)
SM depol depends mainly on opening of VGCa2+ channels
Ca2+ channels open more slowly than Na+ channels, so slower uptake and longer duration of AP than skeletal
Contribution of each ion depends of type of muscle e.g. in gut vs. bladder
How can SM cells be like pacemaker cells?
Can be capable of initiating spontaneous electrical activity to generate regular and repetitive oscillation in membrane potential (slow waves)
What are the two mechanisms leading to a rise in intracellular Ca2+ in SM?
1. Membrane depol opens VGCa2+ channels
2. Agonist-induced Ca2+ reease via IP3
Then for both: Ca2+ released from sarcoplasmic reticulum -> Ca2+ calmodulin -> activates myosin-light chain kinase -> MLCK phosphorylates myosin -> increases ATPase activity and allows M to bind A -> contraction
How does SM contract?
Actin slides past myosin pulling on dense bodies -> DB pull on intermediate filmanet networks -> entire muscle fibre contracts (ends pulled towards centre)
What are the 3 triggers for SM contraction?
2. neural stimulation
3. local factors e.g. in certain locations like visceral organ walls, muscle stretching can trigger contraction
What is the mechanism for parasympathetic and sympathetic control of bronchial SM?
What treatments work on each?
Parasympathetic: ACh/M3 type muscarinic receptors. Treatment: short/long acting muscarinic antagonists e.g. ipatropium, tiotropium
Sympathetic: Adrenalin/NA/beta-2 adrenergic receptor. Treatment: long or short acting beta agonists e.g. salmererool, salbutermol