This document summarizes the key characteristics and functions of smooth muscle. Smooth muscle cells are involuntary, spindle-shaped with a single nucleus, and contain more actin than myosin. They lack sarcomeres and striations seen in skeletal muscle. Smooth muscle forms sheets in organ walls, with longitudinal and circular layers involved in peristalsis. It is innervated by the autonomic nervous system and can contract in a slow, graded manner or as a syncytium. Contraction is triggered by calcium binding to calmodulin and activating myosin light chain kinase to phosphorylate myosin heads, forming actin-myosin cross-bridges. Relaxation occurs via myosin light chain phosphatase dephosph

1. Smooth Muscle
• Involuntary in function
• Cells are not striated
• Fibers smaller than those in skeletal muscle
• Spindle-shaped; single, central nucleus
• More actin than myosin
• No sarcomeres
– Not arranged as symmetrically as in
skeletal muscle, thus NO striations.
• Caveolae: indentations in sarcolemma;
– May act like T tubules
• Dense bodies instead of Z disks
– Have noncontractile intermediate filaments
• Slow, wave-like contractions

2. Smooth Muscle
• Grouped into sheets in walls of hollow organs
• Longitudinal layer – muscle fibers run parallel to organ’s long
axis
• Circular layer – muscle fibers run around circumference of the
organ
• Both layers participate in peristalsis

3. Smooth Muscle
• Is innervated by autonomic nervous system (ANS)
• Visceral or unitary smooth muscle
– Only a few muscle fibers innervated in each group
– Impulse spreads through gap junctions
– Who sheet contracts as a unit
– Often autorhythmic
• Multiunit:
– Cells or groups of cells act as independent units
– Arrector pili of skin and iris of eye

4. Properties of Single-Unit Smooth Muscle
–Gap junctions
–Pacemaker cells
with spontaneous depolarizations
–Innervation to few cells
–Tone = level of contraction
without stimulation
–Increases/decreases
in tension
–Graded Contractions
• No recruitment
• Vary intracellular
calcium
–Stretch Reflex
• Relaxation in
response to sudden
or prolonged stretch

5. Chemical Basis for Smooth
Muscle Contraction
• Smooth muscle contains actin filaments contractile machinery are
predominantly composed of α- and γ-actin
• myosin filaments, having chemical characteristics similar to those in
skeletal muscle.
• Smooth muscle does not contain the troponin complex that is
required in the control of skeletal muscle contraction
• Calmodulin - takes on the regulatory role in smooth muscle

6. Physical Basis for Smooth Muscle Contraction
• Large numbers of actin filaments are attached to dense
bodies. Dense bodies are rich in α-actinin
• Some of dense bodies are attached to the cell membrane.
Others are dispersed inside the cell.
• The dense bodies of smooth muscle serve the same role as the
Z discs in skeletal muscle.

7. Calcium sources
•Smooth muscle has two sources of calcium to initiate
contraction;
•Calcium stored in SR of the cells
•Extracellular calcium that can enter muscle via Ca2+
channels on membrane of smooth muscle
•One source does not control the other and a combination
makes longer lasting contractions

8. Ca2+ from the ECF
• Ca2+ enters through VG Ca2+ channels stimulated by depolarising
wave
• Ca2+ ligand gated channels respond to ligands such as epi and other
hormones allowing an influx of Ca2+
Ca2+ from the ICF
• Smooth muscle has a second messenger system used to open the
RYR on the SR instead of depolarisation as in the skeletal muscle
• Receptors of ligands (epi, ACH) are noted as transmembrane
proteins that are G protein coupled
• When activated, they stimulate the G protein to undergo a cascade
of processes that lead to production of inositol triphosphate (IP3)
• This inositol triphosphate stimulates the RYR channels on SR
allowing Ca2+ to enter sarcoplasm from the SR

9. G Proteins coupled Receptor

10. Cont

11. Cont

12. Cont

13. G Protein Coupled Receptor Regulation

14. SECOND MESSENGER INOSITOL TRIPHOSPHATE &
DIACYLGLYCEROL

15. Inositol Triphosphate & Diacylglycerol

16. Smooth Muscle Contraction: Mechanism

17. MOLECULAR BASIS OF CONTRACTION
• The following sequence of events occurs after a rise in cytosolic calcium in a smooth muscle
fiber :
1. Calcium binds to calmodulin,
2. Calcium-calmodulin complex binds to another cytosolic protein, myosin light-chain kinase,
thereby activating the enzyme
3. Active myosin light-chain kinase uses ATP to phosphorylate myosin light chains in the
globular head of myosin.
4. The phosphorylated cross-bridge binds to actin.
• The smooth muscle myosin isoform has a very low maximal rate of ATPase activity, on the
order of 10 to 100 times less than that of skeletal muscle myosin.
• Since the rate of ATP splitting determines the rate of cross-bridge cycling and thus shortening
velocity,

18. RELAXATION
• To relax a contracted smooth muscle,
• Activated Myosin must be dephosphorylated because dephosphorylated myosin
is unable to bind to actin.
• Dephosphorylation is mediated by myosin light-chain phosphatase, which is
continuously active in smooth muscle during periods of rest and contraction.
• When cytosolic calcium rises, the rate of myosin phosphorylation by the
activated kinase exceeds the rate of dephosphorylation by the phosphatase,
and the amount of phosphorylated myosin in the cell increases, producing a rise
in tension.
• When the cytosolic calcium concentration decreases, the rate of
dephosphorylation exceeds the rate of phosphorylation, and the amount of
phosphorylated myosin decreases, producing relaxation.

19. Latch Mechanism for Prolonged Holding of Contractions
of Smooth Muscle.
• Once smooth muscle has developed full contraction, the amount of
continuing excitation usually can be reduced to far less than the initial
level, yet the muscle maintains its full force of contraction.
• Further, the energy consumed to maintain contraction is often
minimal, economic utilization of ATP.
• The importance of the latch mechanism is that it can maintain
prolonged tonic contraction in smooth muscle for hours with little use
of energy.

20. Comparisons Among Skeletal, Smooth, and
Cardiac Muscle

21. THANK YOU
Dr. Phiri S B