308
UNIT 2
Covering, Support, and Movement of the Body
9
Energy Efficiency of Smooth Muscle Contraction
Smooth muscle takes 30 times longer to contract and relax than
does skeletal muscle, but it can maintain the same contractile
tension for prolonged periods at less than 1% of the energy cost.
If skeletal muscle is like a speedy windup car that quickly runs
down, then smooth muscle is like a steady, heavy-duty engine
that lumbers along tirelessly.
Part of the striking energy economy of smooth muscle is the
sluggishness of its ATPases compared to those in skeletal mus-
cle. Moreover, smooth muscle myofilaments may latch together
during prolonged contractions, saving energy in that way as
well. Smooth muscle cells may maintain that
latch state
even
aFer myosin is dephosphorylated.
±e smooth muscle in small arterioles and other visceral
organs routinely maintains a moderate degree of contraction,
called
smooth muscle tone
, day in and day out without fatiguing.
Smooth muscle has low energy requirements, and as a rule, it
makes enough ATP via aerobic pathways to keep up with the
demand.
Regulation of Contraction
±e contraction of smooth muscle can be regulated by nerves,
hormones, or local chemical changes. Let’s briefly consider each
of these methods.
Neural Regulation
In some cases, the activation of smooth
muscle by a neural stimulus is identical to that in skeletal mus-
cle: Neurotransmitter binding generates an action potential,
which is coupled to a rise in calcium ions in the cytosol. How-
ever, some types of smooth muscle respond to neural stimula-
tion with graded potentials (local electrical signals) only.
Recall that all somatic nerve endings, that is, nerve endings
that excite skeletal muscle, release the neurotransmitter ace-
tylcholine. However, different autonomic nerves serving the
smooth muscle of visceral organs release different neurotrans-
mitters, each of which may excite or inhibit a particular group
of smooth muscle cells.
±e effect of a specific neurotransmitter on a smooth muscle
cell depends on the type of receptor molecules on the cell’s sar-
colemma. ²or example, when acetylcholine binds to ACh recep-
tors on smooth muscle in the bronchioles (small air passageways
of the lungs), the response is strong contraction that narrows
the bronchioles. When norepinephrine, released by a different
type of autonomic nerve fiber, binds to norepinephrine receptors
on the
same
smooth muscle cells, the effect is inhibitory—the
muscle relaxes, which dilates the bronchioles. However, when
norepinephrine binds to smooth muscle in the walls of most
blood vessels, it stimulates the smooth muscle cells to contract
and constrict the vessel.
Hormones and Local Chemical Factors
Some smooth mus-
cle layers have no nerve supply at all. Instead, they depolarize
spontaneously or in response to chemical stimuli that bind to
G protein–linked receptors. Other smooth muscle cells respond
to both neural and chemical stimuli.
Several chemical factors cause smooth muscle to contract
or relax without an action potential by enhancing or inhibiting
P
i
P
i
1
Calcium ions (Ca
2+
)
enter the cytosol from
the ECF via voltage-
dependent or voltage-
independent Ca
2+
channels, or from
the scant SR.
2
Ca
2+
binds to and
activates calmodulin.
3
Activated calmodulin
activates the myosin
light chain kinase
enzymes.
4
The activated kinase enzymes
catalyze transfer of phosphate
to myosin, activating the myosin
ATPases.
5
Activated myosin forms cross
bridges with actin of the thin
filaments. Shortening begins.
ATP
P
i
P
i
Extracellular fluid (ECF)
ADP
Ca
2+
Ca
2+
Ca
2+
Plasma membrane
Sarcoplasmic
reticulum
Inactive calmodulin
Inactive kinase
Inactive
myosin molecule
Activated (phosphorylated)
myosin molecule
Activated kinase
Activated calmodulin
Cytoplasm
Thin
filament
Thick
filament
Figure 9.28
Sequence of events in excitation-contraction
coupling of smooth muscle.
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