Transcript Contraction and Excitation of Smooth Muscles Arsalan Yousuf

Contraction and Excitation of
Smooth Muscles
Arsalan Yousuf
BS 4th Semester
• Involuntary non-striated muscles.
• Much smaller than skeletal
muscles.
• Found in blood vessels, in
lymphatic vessels, the urinary
bladder, uterus, male and female
reproductive tracts,
gastrointestinal tracts, respiratory
tracts, arrector pili of the skin,
ciliary muscle and iris of the eye.
• Same principles of contraction and
relaxation apply with different
physical arrangements
Smooth Muscle Types
Smooth muscles can be divided into two
major types:
• Multi unit smooth muscle (operates
independantly, innervated by single
nerve fiber).
– E.g. ciliary and iris muscle of the eye and
Arrector pili muscles of the skin.
• Unitary smooth muscle (operates
together as a single unit). Also called
syncyctial and visceral smooth muscles.
– Found in walls of gut, bile ducts, ureters,
uterus and blood vessels.
Smooth muscle contraction
Actin and myosin filaments interact
with each other the same way like
in skeletal muscles.
•Contractile process is activated by Ca2+
•Energy for contraction is yielded from
ATP breakdown.
•No troponin complex in smooth muscles.
•Myosin filaments have what are called
“sidepolar” cross-bridges
Smooth Muscles
Smooth Muscle Contraction as compared to
Skeletal Muscle Contraction
• Slow cycling of myosin cross bridges along actin filaments. (1/10 to 1/300)
• Slow ATPase activity
• Cross bridges remain attached for a longer period of time promoting longer time for
contraction
• Small energy is required for sustained contraction (1/10to1/300 of skeletal muscles)
• Slow onset of contraction and relaxation.
• Greater force for muscle contraction (4-6 kg/cm2)
Skeletal muscles
Smooth muscles
The Latch Mechanism
• Prolonged holding of smooth muscle
contractions with little use of energy and little
excitatory signal.
• Prolonged tonic muscle contractions can
remain for hours.
Molecular Mechanism of Smooth Muscle Contraction
In place of troponin, smooth muscle cells contain a large amount of
another regulatory protein called calmodulin.
CONTRACTION
1. Action potential causes depolarization of smooth muscle membrane
2. Voltage gated calcium channels open
3. Increased Ca2+ enters the cytoplasm through sarcoplasmic reticulum.
4. Calcium binds with Calmodulin and then forms a complex with enzyme called
calmodulin-myosin light chain kinase.
5. The enzyme complex breaks up ATP into ADP and transfers the Pi directly to myosin.
6. This Pi transfer activates myosin.
7. Myosin forms crossbridges with actin (as occurs in skeletal muscle).
Figure from Skeletal Muscle contraction lecture
RELAXATION
1. Calcium is pumped out of the cell
2. Myosin Light Chain Phosphatase (MLCP) is activated.
3. Mysoin is dephosphorylated and disassociates from actin causing relaxation
The Latch Mechanism
• Prolonged holding of smooth muscle contractions
with little use of energy and little excitatory signal.
• Prolonged tonic muscle contractions can remain for
hours.
Low number of sarcoplasmic reticulum
resulting in longer contraction time
Calmodulin
• Calcium binding messenger protein expressed in all eukaryotic cells.
• CaM mediates many crucial processes such as:
• inflammation, metabolism, apoptosis, smooth muscle contraction,
intracellular movement, short term and long term memory and
immune response.
• CaM can also make use of the calcium stores in the endoplasmic reticulum
and the sarcoplasmic reticulum.
Neuromuscular Junctions in Smooth Muscles
• Nerve fibers form diffuse
junctions, that secrete
neurotransmitters onto the
muscle matrix.
• Nerve fibers innervate the outer
layer of smooth muscles
• Transmitter substances secreted
by autonomic nerves in smooth
muscles are :
• Acetylcholine
• Norepinephrine and others.
Nervous and Hormonal Control of Smooth
Muscle Contraction
• Transmitter substances secreted by nerves are :
– Acetylcholine
– Norepinephrine
When acetylcholine excites, norepinephrine inhibits, when NE excites
acetylcholine inhibits it
Membrane Potentials and Action Potentials in Smooth Muscles
Action potentials in unitary smooth muscles occur in two forms:
• Spike potentials
• Action potentials with plateaus
Spike Potentials: Duration is 10 to 50 mS.
They can be generated by electrical
stimulation, hormones, neurotransmitters,
stretch, spontaneously on its own.
Action Potentials with Plateaus:
Longer duration, Delayed repolarization,
results in prolonged contraction
Membrane Potentials and Action Potentials in Smooth Muscles
• More voltage gated Ca2+ channels as compared to voltage gated Na+ channels
• Flow of Ca2+ ions into the cell is mainly responsible for generation of action
potentials.
• Ca2+ channels open slowly and remain open for a longer duration resulting in
prolonged plateau of action potentials an muscle contractions.
SLOW WAVE RYTHM
Not an action potential itself
Caused mainly due to slow and rapid pumping of
positive ions, presumably Na+.
Slow waves are also called “pacemaker waves”.
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Smooth Muscle Contraction without Action Potentials
• Transmitter substances cause depolarization, this in turn elicits
contraction. E.g. iris of the eye.
• Smooth muscle fibers are too small to generate an action potential.
• When action potentials are elicited in visceral unitary smooth muscle, 30
to 40 smooth muscle fibers must depolarize simultaneously before a selfpropagating action potential ensues.
• In small smooth muscle cells the local depolarization caused by the nerve
transmitter substance itself spreads “electrotonically” over the entire fiber
and is all that is needed to cause muscle contraction.
• Action potentials can also be generated due to smooth muscle stretch,
e.g. contractions in the gut.
Effect of local tissue factors and
hormones
• Effect of O2 and CO2 concentrations on vasodilation.
• Hormones like epinephrine, norepinephrine, acetylcholine,
angiotensin, endothelin, vasopressin, oxytocin, serotonin and
histamine can affect smooth muscle contraction.