Excitability & Contractility

of Smooth Muscle Cells

Presented by – Hariom Garg

Roll No. - 59
 Introduction
 For Simplicity, smooth muscle can be divided into TWO major types.

1. Single unit/Syncytial/Visceral smooth muscle

• Major control by non – nervous stimuli (intrinsic rhythmic

• Present in wall of most viscera
• Eg. – GI tract, bile duct, ureter, uterus, many blood vessels.

2. Multi unit smooth muscle

• Control mainly by nerve signals

• Eg. – Ciliary & Iris muscle of eye, piloerector muscle
Electrical Properties (Excitability)
 Smooth muscle react to variety of stimuli -
Spike Multiple Spikes
1. Neural
2. Hormonal
3. Chemical
4. Cold
5. Stretch

 Membrane potential of smooth muscles is variable with an

average of -50 mV

 Multi unit smooth muscle do not discharge spontaneously, also

they do not respond to stretch.
Prolonged plateau
 Shape of action potential may be spike, prolonged plateau,
multiple spikes.
 Action Potential
 The action potentials are generally of low amplitude(about 60 mV)

 Opening of Vg Ca2+ channels Influx of Ca2+ from ECF

Depolarization occurs.

 Upstroke of actions potential is prolonged.

 Closure of Ca2+ channels (slowly) Repolarization occurs.

 Opening of Vg K+ channels contributes in later part of

repolarization.
Junction Potential
 Action potential is not observed in multi unit smooth
muscle cells.
Neurotransmitter release

Local depolarization (junction potential)

Spread along the muscle fibers

Membrane potential

Vg Ca2+ channel open

Ca2+ influx
Contraction
Pacemaker Potential

 It recorded in visceral smooth muscle

 Pacemaker activity is not generated at a fixed location

rather it shifts from place to place.

 In visceral smooth muscles it occur at several sites at the

same time & travel for a short distance in the muscle.
 Role Of Calcium
 Different changes in cytosolic calcium concentration produces different
degrees of contraction.
Na+-Ca2+
Vg Ca2+ channel
antiport
Mechanism of Contraction
• MLCK- Myosin light chain kinase. It is a Ca2+ influx into the
smooth muscle cell
Ca2+ –calmodulin-dependent protein
kinase.
Binding of Ca++ with
calmodulin-dependent MLCK
• When calmodulin binds with four
calcium ions, MLCK is activated.
Phosphorylation of myosin
• Calmodulin is a small protein
associated with MLCK.
Increased myosin ATPase activity
• MLCP- Myosin light-chain
phosphatase. Energized myosin head
(Myosin-ADP-Pi complex)
• In smooth muscles, the process of
contraction is myosin-based Myosin binds with actin resulting
(myosin-linked regulation) in cross-bridge formation
 Contraction of muscle Latch-bridge
Mechanism

Dephosphorylation Dephosphorylation of myosin by MLCP

of myosin by MLCP ( cytosolic Ca2+ level)

Decrease myosin ATPase

Cross-bridge remain attached
activity
Called Latch-bridge state
(Sustained Contraction)
Energized myosin head
not form

Cytosolic Ca2+ level

Cross-bridge detaches (Below 10-7 M)

Relaxation Relaxation

Phasic Contraction: All parameters

Tonic Contraction
returns to resting value
 Mechanism of Relaxation
 MLCP is constantly active during the periods of relaxation or contraction
 Rate of MLCK-induced phosphorylation Rate of MLCP-induced dephosphorylation
 Then Phosphorylated myosin in cell Contraction proceed
When, Cytosolic Ca2+ level

Ca2+ detached from calmodulin

Phosphorylation &
MLCK activity
Dephosphorylation of the
myosin are regulated by
respective rise & fall of
Activity of MLCP predominates
cytosolic Ca2+ level.

Dephosphorylation of myosin

Myosin ATPase remains inactive

Relaxation ensues
Neural & Hormonal Influences
 Smooth muscles are supplied by Autonomic nervous system (ANS).
 The visceral smooth muscles have pacemaker activity; any stimulus acting on it
only alters the rate & pattern of action potential formed.

 Parasympathetic Control
 Parasympathetic stimulation is excitatory. It releases acetylcholine(Ach) which i
stimulatory.
 Membrane potential tissue become more excitable.
 Frequency of action potential No. of rhythmic contraction.
 Ach acts by cytoplasmic Ca2+ level.
Sympathetic Control

It is inhibitory. It releases catecholamines.

Membrane potential & frequency of spikes relaxation of muscle.

Norepinephrine(NE) acts through both alpha & beta receptors.

Action through alpha receptors: Action through beta receptors:

NE increases Ca2+ efflux NE stimulates adenylyl cyclase

Activates enzyme cAMP-

Cytosolic Ca2+ level Formation of cAMP
dependent protein kinase

Relaxation Activity of MLCK

Ca2+ uptake by SR
Cross-bridge
Cytosolic Ca2+ level formation

Relaxation
 The multiunit smooth muscles do not have inherent muscle
tone.
 In response to the stimulus of ANS, their Contraction is
regulated in a precise, graded fashion.
THANK YOU