Lecture 13 Smooth And Cardiac Muscle Flashcards
Smooth muscle
Types: visceral and multiunit
Lack visible cross striations
Spindle shaped cells w/single nucleus
Cells usually arranged in sheets within muscle
No z line present - dense bodies
Diff function to skeletal muscle
No troponin or tropomyosin blocking cross bridges - light chains of proteins are attached to head of myosin molecules near “neck” region
Organisation of thick and thin filaments in smooth muscle cell
3 types of filament
Thick myosin
Thin actin
Filaments of inbetween size - part of cytoskeletal framework supporting cell shape
Myosin can only interact with actin when it’s light chains are phosphorylated
Arrangement of filaments
Thick and thin filaments are at slight diagonal from side to side in SM cell
Form a diamond shaped lattice
Myosin molecules arranged in thick filaments so cross bridges are present along entire length
Initiation of contraction
Triggered by Ca2+ dependent phosphorylation of myosin
Ca2+ binds to calmodulin which activates a kinase enzyme
This phosphorylates myosin activating myosin ATPase and hence myosin can interact with actin
Myosin is dephosphorylated by myosin light chain phosphatase
Ca2+ initiates contraction
Ca2+ is released from SR ( not as much as in skeletal) enters cell through membrane channels (voltage/ligand gated)
No T tubule system in smooth SR
Ca2+ removal is slow so longer contraction
Graded response
Role of Ca2+ in skeletal Vs smooth muscle
Smooth
Muscle excitation
Rise in cytosolic Ca2+ (mostly from extracellular fluid)
Series of biochem events
Phosphorylation of myosin in thick filament
Binding of actin and myosin at cross bridges
Contraction
Skeletal
Muscle excitation
Rais in cytosolic Ca2+ (entirely from intracellular SR)
Physical repositioning of troponin and tropomyosin
Uncovering of cross bridge binding sites on actin thin filament
Binding of actin and myosin at cross bridges
Contraction
2 major types of smooth muscle
Multi unit:
Neurogenic
Made of multiple discrete units - function independently - no gap junctions
Units must be separately stimulated by nerves to contract
E.g. large arteries, large airways, iris of the eye and hair follicles
Single unit:
Myogenic (don’t need nerve stimulation)
Fibres excited and contract as single unit
Gap junctions present
Contraction - slow and energy efficient
Function in syncytium
Found in hollow viscera: GI tract, blood vessels, uterus
Single unit SM may be phasic or tonic
Phasic - contracts in bursts, triggered by AP that lead to inc cytosolic Ca2+
Tonic- often partially contracted at all times “tone” due to relatively low resting potential
Doesn’t show bursts of activity like phasic SM but varies in increments above or below usual tonic state
Factors influencing smooth muscle contractile activity
Spontaneous depolarisation of cells
Signalling molecules - NTs from autonomic neurons and hormones
Local changes in extracellular fluid (pH, O2, osmolarity, ions)
Stretch
Myogenic response to stretch
Vascular smooth muscle cells respond to stretch by contracting
Smooth muscle can continue to develop tension even when considerably stretched
Stress relaxation response
Cardiac muscle
Found in the walls of the heart
Similar striations to skeletal muscle
- fibres joined in branching network
- z lines present
Cells joined at intercalated discs
T-tubule system
Innervated by autonomic nervous system
Cardiac muscle resting potential
Resting membrane potential approx 90mV
AP generated intrinsically
Functions as one unit
Each AP triggers full contraction followed by relaxation (can’t grade force contraction like skeletal muscle)
Cardiac muscle action potential
Spontaneous rapid depolarisation of cells occurs
Plateau phase
Slow repolarisation
Rhythmic firing
SA (sinoatrial) and AV (atrioventricular) nodes
Firing rate controlled by sympathetic and parasympathetic nervous systems
Firing of pacemaker cells
Movement of Na+ K+ and Ca²+ via ion channels
At -60mV Na channels open and slow inward current
Slow depolarisation (prepotential) Ca²+ channels open - depolarization
K+ channels open - repolarisation then when closed followed by slow depolarization (prepotential)
Pacemaker activity
Intrinsic automaticity of SAN = 100-110bpm
Activity of SAN normally controls heart rate
Nervous and hormonal control of SAN/AVN
AVN capable of independent activity
Latent pacemaker located in the conduction system e.g. Purkinje fibres can take over if SAN and AVN fail