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Chapter 10: Smooth Muscle
Characteristics
--Size:
*smaller than skeletal (30x smaller diameter, 1000x smaller length)
--uninucleated
--not striated
--involuntary
--hormonal and neuronal regulation
*skeletal is exclusively neuronal
--Autonomic innervation
*skeletal is somatic
--Varicosities
*skeletal have end bulbs
--Neurotransmitters: Ach and norepinephrine
*can be excitatory or inhibitory
*Ach is ALWAYS excitatory for skeletal
*Ach is ALWAYS inhibitory for cardiac
--not all smooth is innervated
--autorhythmic activity
--Location:
*visceral
*blood vessels
--Two Types of Smooth Muscle
a. Unitary/Single Unit Smooth Muscle
*many fibers contract as a single unit
*fibers are aggregated in sheets or bundles
*cell membranes are adherent (no insulation)
*gap junctions-syncytial (autorhythmicity)
*non-nervous control can stimulate the syncytium
*Examples: visceral organs
b. Multi Unit Smooth Muscle
*each fiber is a discrete unit (contracts independently of others)
*fibers are covered (insulated)
*neural control: no autorhythmicity
*Examples: ciliary and iris muscles, piloerectors (intrinsic eye mm.)
*endomysium
--Anatomy
a. Caveoli: no t-tubules, replaced by these
b. rudimentary SR: very little Ca++ storag, most CA++ comes from
extracellular fluid
c. Dense bodies: on cell membrane and inside, attachments of actin,
attachment of neighboring cells
*Analogous to Z-disk of sarcomeres of skeletal muscle
*myosin filaments form sidepolar cross bridges that enables smooth
m. cells to contract as much as 80% (vs. 30% for skeletal)
d. Calmodulin: binds Ca++ (NO troponin in smooth muscle)
e. Diffuse Junctions: NT diffuse over superficial fibers)
*no NMJ
--Latent Period
*the time needed for Ca++ diffusion creates a long latent period (50x greater
than skeletal muscle)
Physiology of Smooth Muscle
--Contraction starts slowly and lasts longer
*no t-tubles and very little SR
*Ca++ must flow in from outside
--calmodulin replaces troponin
*Ca++ binds to calmodulin
*Ca++/calmodulin complex activates MYOSIN LIGHT CHAIN KINASE
*myosin light chain kinase phosphorylates the myosin head so contraction
can occur  enzyme works slowly, slowing contraction
--a single contraction cycle can be 10-30x longer than skeletal
--the energy used to sustain a contraction is 1-300x less than skeletal
--the force of contraction is 1-2x greater than skeletal
--Latch mechanism:
*maintains prolonged (hours to days) tonic contraction with very little
energy expenditure
--Stress-relaxation and reverse stress-relaxation of all hollow organs
--depolarization leading to AP is mostly due to Ca++ influx (no Na+)
*extra cellular calcium has great effect on smooth
--Smooth Muscle Action Potentials
a. Normal AP (skeletal like)
b. Spike potentials on top of slow wave potentials (autorhythmicity)
c. Plateau potentials (cardiac like)
**Unitary smooth: has spike/slow wave, and plateau
**Multi-unti: d/n generate AP, has electrotonic conduction
--Resting Membrane Potentials
*RMP of smooth is about 30mV less than skeletal and the threshold potential
is much higher (-30mV)
Regulation of Contraction
--Nerve signals from autonomic nervous system
--Changes in local conditions (pH, O2, CO2, temp, and ionic concentracions) 
dominant regulation
--hormones: epinephrine (relaxes muscle in airways and some blood vessels)
--Stress-relaxation response
a. when stretched, initially contracts and then tension decreases to what is
needed
b. stretch hollow organs as they fill and yet pressure remains fairly constant
c. when empties, muscle rebounds and walls firm up
Regeneration of Muscle
--Smooth muscle fibers
*regeneration is possible
*cells can grow in size (hypertrophy)
*some (uterus) can divide (hyperplasia)
*new fibers can form from stem cells in BV walls
--Skeletal Muscle Fibers
*cannot divide after 1st year
*growth is enlargement of existing cells (hypertrophy)
*repair: satellite cells and bone marrow produce some new cells
--Cardiac Muscle Fibers
*cannot divide or regenerate
*all healing done by fibrosis (scar formation)