3.9 smooth muscle physiology
TRANSCRIPT
DR NILESH KATE
MBBS,MD ASSOCIATE PROF
DEPT. OF PHYSIOLOGY
SMOOTH MUSCLE
PHYSIOLOGY.
OBJECTIVES. Functional Anatomy & Organization Process of Excitability & Contraction. Characteristics of Excitability & Contractility. Excitation & Inhibition.
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FUNCTIONAL ANATOMY & ORGANIZATION
Non-striated Muscle. Involuntary muscle. Long fusiform in
bundles or fasciculi.
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TYPES OF SMOOTH MUSCLES Single unit smooth
muscle Muliti unit smooth
muscle.
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SINGLE UNIT SMOOTH MUSCLE Visceral smooth
muscles Present in hollow
viscera like GIT, Uterus, Ureter, Urinary Bladder & Respiratory tract.
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SALIENT FEATURES Arranged in large sheet. Has low resistance bridges
(Gap Junctions) between individual muscles.
Function in a Syncitial fashion & contract as a single unit.
Has their own Rhythmic contractility ( Myogenic Tone)
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SALIENT FEATURES Rate of contraction
determined by Pacemaker region & Nerve supply only Modulates its activity.
Contraction is stimulated by Stretching involved in Autoregulation of blood flow.
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MULTI UNIT SMOOTH MUSCLES
Made up of Multiple units without interconnecting bridges-Non-Syncitial.
Location – Blood vessels, Epididymis, Vas deference, Iris, Ciliary body & Piloerector muscle.
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SALIENT FEATURES Multi-unit muscle each
innervated by single nerve ending.
Contraction is Neurogenic & each stimuli causes irregular Tetanic contraction.
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SALIENT FEATURES Do not show
spontaneous contraction – No Pacemaker activity.
No Gap Junction so excitation localized within motor unit.
Do not respond to stretch.
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Innervations of smooth muscles Nerve supply –
Autonomic both Sympathetic & Parasympathetic.
Symp – Contraction & Parasymp – Relaxation.
Preganglionic fibres – ganglion – postganglionic fibres – muscle.
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Neuromuscular junction of Smooth Muscles
Post ganglionic fibres branch extensively.
Neuronal network has Beaded appearance due to varicosities.
Varicosities contains chemical neurotransmitter (Ach/NE)
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Neuromuscular junction of smooth muscles
Nerve fibres do not end in Motor End Plate but releases its neuro-transmitter in interstitial fluid near muscle fibre.
It then diffuses in muscle fibre & causes activation.
So single stimuli will not cause activation of entire muscle Multiple Stimuli are required.
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Excitatory Junctional Potential (EJP) or Inhibitory Junctional potential
(IJP) Either depolarizing or
repolarizing responses are recorded in response to stimuli.
These potentials Summate with repeated stimuli
EJP & IJP are local responses.
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STRUCTURE OF SMOOTH MUSCLE FIBRE
Spindle shaped cells with broad central part & tapering ends.
Length & diameter varies with organ GIT – 30-40 mm/5 mm
diameter. Blood vessels – 15-20
mm/2-3 mm. Uterus – 300 mm /10 mm
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SALIENT FEATURES OF STRUCTURE OF SMOOTH MUSCLE FIBRE
Plasma membrane – surrounded by Externa Lamina. Cell communicate through Gap Junction.
Sarcoplasm Nucleus – Central/Oval Contains Mitochondria, Golgi apparatus, Endoplasmic
Reticulum, Ribosomes. Sarcoplasmic reticulum – similar to skeletal
muscle but not as developed.
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SALIENT FEATURES OF STRUCTURE OF SMOOTH MUSCLE FIBRE
Myofibrils- Sarcotubular system & triad not well developed.
Less thick filaments & More thin filaments.
Z line not well developed. Actin – Troponin is absent Myosin – bind only if
phosphorylated.
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SALIENT FEATURES OF STRUCTURE OF SMOOTH MUSCLE FIBRE
Dense bodies – attached to the cell membrane
Actin filaments are attached to dense bodies.
When muscle contracts dense bodies are drawn close to each other.
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PROCESS OF EXCITABILITY & CONTRACTILITY.
PROCESS OF MUSCLE EXCITATION PROCESS OF EXCITATION CONTRACTION
COUPLING PROCESS OF MUSCLE CONTRACTION.
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PROCESS OF MUSCLE EXCITATION
Electrical activity in single unit (Visceral) smooth muscles. Resting membrane potential Action potential
Spike potential Spike potential superimposed over slow wave
potentials. Action potential with plateau.
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RESTING MEMBRANE POTENTIAL
Range between - -50mv to -75mv
Peculiarity – Unstability – keeps on oscillating between -55 to -35mv.
Oscillations due to – Superimposition by pacemaker potential due to rhythmic change in Ca channel permeability & activity of Na-K Pump.
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ACTION POTENTIAL When depolarization
reaches threshold action potential begins & transmitted to other muscle cells through Gap junctions.
3 types action potential Spike potential Spike potential over
pacemaker potential Action potential with plateau.
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SPIKE POTENTIAL Similar to skeletal
muscle except Duration – 10 to 50 msec Amplitude – very low Do not reach Iso-electric
base. Occur in response to
electrical stimulation, hormone, neurotransmitter & stretch of smooth muscle.
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SPIKE POTENTIAL OVER PACEMAKER POTENTIAL
Slow wave rhythm called Pacemaker waves seen in GIT
These cannot cause muscle contraction but when potential rises above -35mv action potential develop.
Appear rhythmically & causes contraction of muscle fibre.
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ACTION POTENTIAL WITH PLATEAU.
Seen in ureter, uterus & vascular smooth muscle.
Like in skeletal muscle there is rapid depolarization but Repolarization is delayed by 100-150msec.
This prolonged depolarization is responsible for sustained contraction of certain smooth muscle.
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Ionic basis of action potential. Depolarization – due to entry of
Ca rather than Na. This muscle has more voltage
gated Ca channels than Na channels.
These open & close slowly & responsible for prolonged action.
Ca along with depolarization also causes contraction of smooth muscle.
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Electrical activity in multiunit smooth muscles.
Multi-unit smooth (Iris & Piloerector) muscle
respond to nerve stimulation which releases Ach &
NE.
These do not generate AP but causes excitatory
Junctional Potential (EJP) & spread to entire fibre.
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PROCESS OF EXCITATION CONTRACTION COUPLING
Electro-Mechanical coupling. Pharmacomechanical coupling. Mechano-Mechanical coupling.
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ELECTRO-MECHANICAL COUPLING.
When smooth muscle are excited through depolarization – voltage gated Ca channels open – Ca ions enters into Sarcoplasm – stimulate more release of Ca ions – Ca induced Ca release.
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PHARMACOMECHANICAL COUPLING.
Smooth muscle are excited by chemical agents
Mechanism – Chemicals (NT & Hormone)
bind to Ligand gated Ca channels & open it – influx of Ca
Chemicals bind to membrane receptors –activate second messengers of G protein- through IP3 causes release of Ca ions.
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MECHANO-MECHANICAL COUPLING.
Muscles are excited by stretch – stretch sensitive Ca channels open & causes influx of Ca from ECF.
Ca bind with calmodulin & this complex initiate muscle contraction.
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PROCESS OF MUSCLE CONTRACTION.
Molecular mechanism is similar to skeletal muscle
but..
Smooth muscle don’t contain Tropomyosin &
Troponin.
Light chain of Myosin acts as Tropomyosin & called
Regulatory chain of Myosin.
Ca binding protein Calmodulin acts as Troponin.
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STEPS OF CROSS-BRIDGE CYCLING.
Ca combine with Calmodulin – forms complex – activates enzyme Myosin Light Chain Kinase (MLCK)
Phosphorylation of the Myosin Regulatory chain.
Myosin head acquires capability to bind with actin & forms Cross-bridging.
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STEPS OF CROSS-BRIDGE CYCLING.
Power stroke – formation of Actin-Myosin ADP Pi complex – confirmational change in myosin head- flex towards arm – generate mechanical force i.e. Power Stroke. Actin slide over myosin & causes contraction Dense bodies are same as Z line.
Relaxation of smooth muscle – Ca pump removes Ca from ICF to ECF – reverse all stages except Phosphorylation of Myosin.
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CHARACTERISTICS OF EXCITABILITY & CONTRACTILITY. Slow excitation-contraction coupling. Plasticity. Latch phenomenon. Marked shortening of smooth muscle durin
contraction. Energy required to sustain smooth muscle
contration.
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Slow Excitation-contraction coupling.
Smooth muscle contraction starts after 200 msec
after spike
Peak of contraction reach after 500 msec.
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PLASTICITY. Can Readjust its
resting length. Thus it not follows
length tension relationship that is valid for striated muscle.
So length tension relationship curve is Jagged line.
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LATCH PHENOMENON. Mechanism by which
smooth muscle maintain high tension without actively contracting.
Allows long term maintenance of Tone.
So muscle can not generate active tension but Resists passive stretching.
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LATCH PHENOMENON. Since smooth muscle found
mainly in hollow viscera that should resists stretching.
CAUSE – Both myosin kinase & myosin phosphatase enzyme strongly activated, cycling frequency of myosin head & velocity of contraction increases.
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LATCH PHENOMENON. As this activation & cycling
frequency decreases – lower activation of enzymes causes myosin head to remain attached to actin for longer time with less energy expenditure as ATP is required for detachment.
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Marked shortening of smooth muscle durin contraction.
A smooth muscle can contract more than 2/3rd its stretched length while skeletal muscle contract up to 1/3rd.
This allows viscera to change diameter from large to almost zero.
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Energy required to sustain smooth muscle contraction.
Energy is much less than skeletal
muscle as attachment cycling of cross
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EXCITATION & INHIBITION. Excitation –
Multi Unit Smooth Muscle – stimulated through nerves
Single Unit Smooth Muscle – through Nerves, Hormones, Pacemakers, Stretching, Cold Temeprature.
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FUNCTIONS Control movement of material through most
of hollow organs Propel material in GIT Control blood flow in arterioles. Expell material from bladder. Control Piloerection Iris control.
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INHIBITION OF SMOOTH MUSCLE
Through nerves by Sympathetic
Stimulation. e.g. – Intestinal smooth
muscles.
Through Hormones – Progesterone
decrease activity of uterus.
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Thank You
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