Smooth muscle

• Smaller, spindle shaped fibers (1-5micrometer in

diameter & 20-50 micrometer in length)
• Single nucleated
• Non striated
• Irregular arrangement of contractile filament
• Poorly developed sarcoplasmic reticulum
• Few mitochondria
• Depend on glycolysis for their metabolic needs
Types of smooth muscle
• Multi unit smooth muscle & Single unit smooth
muscle
 Multi-unit smooth muscle
• Individual cell separates
• No gap junctions
• Shows fine graded contractions
• Each fiber can contract
independently of the others
• Nerve regulated
• Location- iris, ciliary muscles of
eye, walls of large blood vessels
 Visceral smooth muscle ( single unit)
• Arranged in sheets /bundles
• Gap junctions(low resistance
bridges)
• Functions as syncytium
• Shows all or none law
• Nerve regulated- modify the
activity
• Location- walls of hollow
visceral organs- GIT, uterus,
urinary bladder, blood vessels
 Nerve supply
Dual nerve supply :Sympathetic &
parasympathetic
• Pre & post ganglionic neurons
• Stimulatory/ inhibitory
• Neurotransmitters- Ach,
noradrenaline
• Receptors- Ach- muscarinic receptors
• Noradrenaline- adrenergic α /β
• Stimulation/ inhibition- depending on
receptors
• NMJ – not well developed
• Axons- branched- swollen regions-
varicosities
Similarities with skeletal muscle.
• Actin and myosin filaments interact with each other
• contractile process is activated by calcium ions
• ATP is degraded to ADP to provide the energy for
contraction
Major differences
• physical organization of smooth muscle
• excitation-contraction coupling
• control of the contractile process by calcium ions
• duration of contraction
• amount of energy required for contraction
 Physical organization of smooth muscle
• Actin & myosin filaments
• No troponin- but has calmodulin
• No sarcomere
• Dense bodies: attached to cell membrane /
dispersed inside the cell.
• Actin filaments attached to dense bodies
(No Z- lines) /
• Membrane- dense bodies of adjacent cells –
bounded together by intracellular protein
bridges
• Through these bonds force of contraction
transmitted from one cell to the next
Contractile unit- between two
dense bodies
• Large number of actin filaments
radiating from two dense bodies
• Actin filaments overlap myosin
filament
• Actin- 5-10 times more than
myosin
• Myosin- diameter -twice that of
the actin
Sequence of events in smooth muscle contraction
& relaxation
 Regulation of Contraction by Calcium Ions
Initiating stimulus for contraction - increase in intracellular calcium ions
• Source of Calcium - ECF, sarcoplasmic reticulum
• ECF : voltage- or ligand-gated plasma membrane channels, depending
on the stimulus
• Intracellular stores: RyR /inositol trisphosphate receptor (IP3R) Ca2+
channels

• Ca++ binds to calmodulin

• Ca++ - calmodulin complex
• Activates myosin light chain kinase
• Phosphorylation of myosin light chain
• Phosphorylated myosin ready to bind to actin
Side polar cross bridges:
On one side- hinge in one direction, other side hinge in
the opposite direction

This mechanism simultaneously pulling actin filament on

two opposite directions- allows smooth muscle to contract
as much as 80% of their length
• Cross bridge cycle- attachment- release and
reattachment – very slow
• Begins to contract -50- 100 ms after it is excited
• A single smooth muscle contraction may last as
long as 3 seconds
• The rate of ATP splitting by myosin ATPase is
much slower, cross bridge activity is very slow
• Relaxation is also very slow ( removal of Ca++
is slow)
• Graded- increased Ca++ ------ increased cross
bridges
 Latch bridge mechanism
• Myosin cross bridges remain attached to actin for
some time, after the cytoplasmic Ca 2+
concentration falls, even after dephosphorylation
• Sustained contraction - latch bridge
• Significance- prolonged tonic contraction for
hours with little use of energy and without fatigue
• Enables smooth muscle to maintain tension with
less ATP consumption
 Properties of smooth muscle
Excitability –unstable RMP (-50 to – 60mv)
• Shows continuous irregular contractions
• Tonus/ tone( state of a partial contraction)
Action potential – 2 forms- spike & action potential with
plateaus
• Typical spike AP- elicited by electrical stimulus,
stretch, actions of hormones, spontaneous generation by
muscle itself
• AP with plateaus- onset similar to spike AP, but
repolarization is delayed for 100- 1000ms (Ca++
channels)
• Accounts for prolonged contraction as in ureter or uterus
Action potentials can be elicited in many ways
• Electrical stimulation
• Action of hormones
• Action of transmitter substances from nerve
fibers
• Stretch
• Spontaneous generation
Typical spike AP
Duration – Slow wave
10 to 50 milliseconds rhythm
and AP

AP with plateau-
prolonged contraction
as in uterus, ureter
 Slow wave potentials leads to action
potential
• Some smooth muscle- self excitatory
• Shows pacemaker activity
• Action potentials with out an extrinsic stimulus
• In the gut – slow waves – local property of
smooth muscle fibers
• Slow waves when strong enough- generates AP
– pumping of positive ions (Na+)
• membrane potential rises -60 to – 35 mv
• Action potential spreads over the muscle and
cause muscle contraction
 Depolarization of multi-unit smooth muscle
• Contract in response to nerve stimuli
• Nerve endings- releases Ach/ noradrenaline
• Depolarization of smooth muscle membrane
• Action potential usually do not develop
• As fibers are too small to generate AP -
• Local depolarization (junctional potential) by
NT spreads “electrotonically” over the entire
muscle fiber
• Results in muscle contraction
 Contractility

• Response to stretch
• Response to circulating chemicals
• Response to thermal stimuli
 Effect of hormones and local factors on
smooth muscle contraction

Neurotransmitters released by ANS

Hormones

Smooth muscle
contraction

Local factors Temperature

Stretch
Stretch :
Stretching of smooth muscle

Opening of mechanosensitive ion channels

Increased movement of Ca++from ECF to cell

Membrane depolarisation

Muscle contraction
• Intestine content
 Local tissue factors

Relaxation of smooth muscle - Vasodilation

• lack of Oxygen in local tissues - hypoxia
• Excess of carbon dioxide
• Increased H+
• Adenosine, Lactic acid, Increased K+, Decreased Ca+
+, increased body temperature
• Nitric acid (NO)- released from nerve terminal/
endothelial cells
• Hormones- noradrenaline, adrenaline,
histamine, angiotensin II, serotonin, ADH,
oxytocin, estrogen and progesterone
Hormones/ neurotransmitter- excitatory-
• Binding to hormone gated excitatory receptors
• Opening of Na+/ Ca2+
• Depolarization – AP -muscle contraction
contraction

• Inhibitory- binding to receptors

• Closure of Na+/ Ca++/ efflux of K+
• Hyperpolarization
• Inhibits muscle contraction
• Hormone + membrane receptor – no
depolarization - Internal changes in the muscle
fiber – contraction/inhibit contraction
• Release of calcium – contraction
• Activate enzyme adenylate cyclase -cAMP
Effect of various agents on smooth muscle
• PLASTICITY
• At any given length, tension exerted by the
smooth muscle varies
• The quality of being plastic – capacity can be
altered
 PLASTICITY

Tension

Length
 Length –tension relationship- plasticity

Stretch a piece of smooth muscle

Increased tension- but after sometime tension

decreases

Decreases even below the level exerted before

stretch
• (urinary bladder- volume increased- pressure
increases- later pressure decreases)