Smooth Muscle: The odd one out

General Facts

• No troponin
• In skeletal and Cardiac muscle this moves tropomyosin
• It’s functional replacement is Calmodulin
• No striations
• Seen in Skeletal and Cardiac
• Dense bodies replace Z lines
• Actin connects to dense bodies by alpha actin
• The proteins stretch across cell at different angles
• Slow and sustained contractions
• Relatively small SR
• Multiple synaptic connections to muscle cell
• In the form of varicosities
• Small swellings of the neuron
• Neurotransmitter gathers
• Muscle membrane much less adapted for synaptic transmission
• Receptors are much more diffuse

There are two main types of smooth muscle:

Unitary/Visceral Smooth Muscle

• Sheet of connected muscle cells
• Adherens junctions keep them together
• Gap junctions help to transmit electrical activity throughout the sheet to give synchronous contractions
• The cells share common innervation
• They are mostly controlled by circulating hormones with some modulation from autonomic nerves
• Stretch increases tone (bayliss myogenic effect)
• Where
• Wall of visceral organs
• GI tract
• Blood vessel
• Respiratory tract
• Can produce action potentials
• Spontaneous contractions

Multi-unit Smooth muscle

• Individual muscle cells not connected by gap junctions
• Contract independently
• Innervated individually
• Some cells are innervated by more than one neuron
• Mostly controlled by nerve with some modulation by hormones
• Some basal tone
• No action potentials
• Where
• Iris
• Piloerector muscles

Membrane Potential

• The resting membrane potential of smooth muscle cells varies a lot
• May be anywhere as negative as -50mV
• The spontaneous contractions may be produced by a pacemaker potential
• Due to time and voltage dependent ion channels
• In cells that do not produce action potentials they can exhibit slow waves
• The membrane potential oscillates over time
• This could be due to Ca and K currents
• At resting Vm voltage gated Ca2+ channels are open
• This Ca2+ influx depolarises the cell
• Positive feedback
• As intracellular Ca2+ levels rise Ca gated K channels begin to open
• The K efflux repolarises the cell and the cycle continues
• There are 3 main different “action potentials”
• Spike
• Longer than in skeletal muscle
• Upstroke is longer
• Ca channels are slower to open than the Na channels in Skeletal and Cardiac
• Repolarisation is also slower
• Slower inactivation of Ca channels
• Slower activation of voltage gated K channels
• Spike + Plateau
• As seen in Cardiac muscle the plateau may last hundreds of milliseconds
• Genitourinary tract
• Again due to longer influx of Ca
• Slow wave + Spike
• May also have spike potentials superimposed on top

Contraction

• Multi unit smooth muscle cannot generate action potentials
• But it will create these slow waves because of excitatory neurotransmitter such as Acetylcholine and Noradrenaline
• This causes a graded depolarisation that is directly related to the contractile force
• The depolarisation opens L-type Ca channels
• The depolarisation can also activate phopholipase C which generates IP3
• IP3 will then bind to SR Ca channels opening them
• This can also happen by a neurotransmitter binding to a g-protein coupled receptor that results in IP3 generation with no depolarisation
• In cardiac and skeletal muscle CICR plays an important role in initiating contraction but it may not happen normally in smooth muscle
• Calmodulin takes the place of troponin in smooth muscle
• 4 Ca ions bind to calmodulin creating the calcium-calmodulin complex
• The Ca-Calmodulin complex activates myosin light chain kinase (MLCK)
• MLCK then phosphorylates MLC
• As a result the myosin head then undergoes a conformational change which increases it’s ATPase activity
• This allows it to interact with actin and form cross bridges
• This is slow to occur