Page: 18a

Smooth muscles:

• Most of Ca++ needed for smooth muscles contraction is coming from ECF
(extracellular fluid) because smooth muscles have poorly developed sarcoplasmic
reticulum.
• Smooth muscles divided into 2 types :( according to presence of gap junctions)
1. Single unit : (more common)
o It is also called viscera
o Presence of gap junctions
o All fibers act as one unit
o Have little innervations: so action potential conduct to the inside of
muscle fibers by gap junctions
o Origin of electrical activity is spontaneous (it has specialized muscle
cells that work as pacemaker, so these cells have leaky type ion (Na+
or K+) channels).
o So the effect of innervations of sympathetic and parasympathetic is
not to make (begin) the contraction but to modify the pacemaker
activity (increase or decrease the rate of contraction )
2. Multi units : (less common)
o Each muscle fiber should receive innervation (like skeletal muscles)
o Innervations of multi units : each nerve (remember autonomic nerve)
give branch and each branch ends with bulges called varicosities
which contain neurotransmitters
o the receptors of neurotransmitter are found all through the muscle
fiber (on the surface of the plasma membrane) not in certain places
(like end plate in skeletal muscles)
o So we don’t have close relation between nerve and receptors, these
synapses called en-passage synapses.
o Type of potential is graded potential, so if we increase the strength
of stimulus we will increase the strength of contraction.
o Examples of multi units smooth muscles :
- Arrector pili muscle (hair muscle): contracted at cold and great
fear situations.
- Ciliary muscle: contraction and relaxation of this muscle will
affect the thickness of lens of the eye which adapts our vision (to
see close or far things)so it is also called adaption muscle.
Page: 18b

• In smooth muscles there is no troponin but there are tropomycin which until today
we don’t know its function.
• Calmodulin is the binding protein of Ca++ in smooth muscles.
• Smooth muscles contraction :Ca++ - calmodulin complex activate myosin light chain
kinase ……… phosphorylation of myosin ……… activate ATPase ……… cause tension
(contraction)
• Relaxation of smooth muscles happens when Ca++ - calmodulin complex is
completely dissociated ( Ca++ separate from calmodulin)
• Smooth muscles can make continuous (sustained) contraction (by latch-bridge
mechanism), we need that to regulate and maintain our blood pressure (especially in
arterioles). And this regulation of blood pressure is done by constriction or dilation
of blood vessels [arterioles] (so sustained contraction (tonic) will allow blood
vessels to do both constriction and dilation) .

Vasodilation vascular tonic vasoconstriction

in arterioles

• Continuous (sustained ) contraction is called smooth muscle tone

• If there wasn’t sustained contraction in arterioles this mean that arteriole
diameter will increase ……… and leads to low blood pressure ……… no blood will reach
to many vital parts of our body (like brain, kidneys ……).
• Smooth muscle contraction needs both Ca++ and ATPase (like skeletal muscles).
• ATPase before the phosphorylation of myosin is inactive (in resting state)

Page: 18c

• Sources of Ca++ in smooth muscles :

o Mainly from voltage gated Ca++ channels.
o Ligand (chemical) gated Ca++ channels. {ECF}
o IP3 gated Ca++ channels (which similar to ligand channels)
o Little from sarcoplasmic reticulum (poorly developed ).{ICF}
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• In smooth muscles thick filaments (myosin) are very long ……… overlap will remain
even in strong stretching ……… maintain of cross bridges ……… maintain of muscle
contraction.
• In smooth muscles thin and thick filaments don’t arrange in sarcomeres
• Dense bodies we can see it through E/M as black bodies , these are found on cell
membrane and in cytoplasm.
• Intermediate filaments in smooth muscles (are attached to dense bodies) : help to
bring dense bodies near to each other while contracting.
• Shortening of smooth muscle while contracting is due to stretching of thin
filaments (actin …) and intermediate filaments to cell membrane through dens
bodies (which are attached to the cell membrane )
• Botulinum toxin : block releasing of ACh from presynaptic terminals (in
neuromuscular junction) …… no action potential ……… no contraction (weakness or
paralyses of muscles )
• The most dangerous muscles to be affected by this toxin are diaphragm and
skeletal muscles of larynx (laryngeal muscles) because this will lead to (respiratory
failure , no breathing then death)
• Curare: was discovered by alhonood al7omor to paralyze preys .
• D-tubocurarine : is a drug used as muscle relaxant for surgeries (anesthesia) for
examples (to open the abdomen easily ) so the doctor after giving this drug to the
patient he must make artificial breathing (relaxation of diaphragm)
• Neostigmine: giving in Myasthenia gravis disease.
• sOOO we give the patient curare before surgery and neostigmine after it (as an
anti-curare)
• ACh reuptake at terminals either as complete ACh or broken (to choline and
acetate), ACh if doesn’t reuptake it will diffuse to the near tissue and finally loss
by urine.
• In neuromuscular junction there is co-transport between Na+ and choline and
hemicholinium prevent this transport so it leads to muscle weakness.

Page : 20

Regeneration of muscle fibers:

• Fibrous tissue has no contractility (so it will cause weakness to the muscles)
• In muscles (when some fibers are damage {dead}): fibroblast will make collagen then
collagen will rearranged and make fibrous tissue (scar) instead of muscle fibers.
• Ischemia can lead to death of cardiac muscle
• There is limited skeletal muscle regeneration: remained embryonic cells
(undifferentiated mesenchymal cells) ………… give myoblast ………… make muscle
fibers.
• 99% of dead muscle tissue is replaced by fibrous tissue.
• Exception is uterus smooth muscles which regenerate under the effect of some
hormones.
• Hyperplasia: increases the no. of muscle fibers.
• Hypertrophy: muscle fibers enlarged (remember no increase in number) due to
increasing of fibrils number and diameter.