3.9 smooth muscle physiology

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DR NILESH KATE MBBS,MD ASSOCIATE PROF DEPT. OF PHYSIOLOGY SMOOTH MUSCLE PHYSIOLOGY.

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Page 1: 3.9 SMOOTH MUSCLE PHYSIOLOGY

DR NILESH KATE

MBBS,MD ASSOCIATE PROF

DEPT. OF PHYSIOLOGY

SMOOTH MUSCLE

PHYSIOLOGY.

Page 2: 3.9 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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