BIO 3520 Notes, 10/13/08
SMOOTH MUSCLE
I. Introduction. [Widmaier, pg. 284]
A. Found mostly in walls of hollow organs and tubes.
B. Involuntary body functions.
C. Under control of autonomic nervous system and circulating hormones.
D. Major function -- To control diameter of hollow organs.
II. Structure of a Smooth Muscle Fiber. [pp. 284-285]
A. Smooth muscle fibers are spindle-shaped (fig. 9-32).
1. Shorter and smaller diameter than skeletal muscle fibers.
2. Single nucleus.
B. Arrangement.
1. Circular arrangement around blood vessels.
2. In most hollow organs -- outer longitudinal layer, inner circular layer
(fig. 15-6).
C. Filaments.
1. Diagonal arrangement of thick and thin filaments (fig. 9-33).
a. No striations.
2. Thin filaments contain actin.
a. Anchored to cytoplasmic bodies called dense bodies or to cell
membrane (no Z lines).
3. Thick filaments contain myosin.
a. Overlap between filaments -- allows smooth muscle fibers to develop
tension over a wide range of lengths.
III. Contraction of Smooth Muscle. [pp. 285-287]
A. Contraction is caused by increased Ca++ level in cytoplasm.
1. Sarcoplasmic reticulum is poorly developed.
2. Most Ca++ enters from extracellular fluid by Ca++ channels in cell
membrane.
3. Ca++ pump slowly removes Ca++ from cell.
B. Contraction of smooth muscle fiber is graded.
C. Regulatory protein is a calcium-binding protein called calmodulin.
D. Power stroke is similar to that of skeletal muscle.
1. Myosin ATPase activity is low compared to skeletal muscle
>tension develops slowly.
E. Tension is maintained with high efficiency by the formation of latch bridges.
F. Smooth muscle requires much less energy than skeletal muscle.
IV. Control of Smooth Muscle Contraction. [pp. 287-289]
A. Capable of self-excitation (table 9-5).
1. Slow wave rhythm of membrane potential.
2. Gradual depolarization, followed by repolarization.
3. Accompanied by mild contraction and relaxation.
4. If depolarized past threshold
> action potential>stronger contraction (fig. 9-36).
B. Stretching will increase rate of depolarization.
C. Sources of control.
1. Hormones may cause contraction or relaxation.
a. Example: Oxytocin causes contraction of uterine smooth muscle.
2. Autonomic nervous system.
V. Autonomic Nervous System. [pp. 180-185]
A. Introduction.
1. Subdivision of motor division of PNS.
2. Innervates cardiac muscle, smooth muscle, and glands.
3. Subject to involuntary control.
4. Motor pathway involves two neurons (fig. 6-43).
a. Synapse is located outside the CNS in an autonomic ganglion.
b. Preganglionic neuron -- cell body in CNS, axon terminal in
gangion.
c. Postgangionic neuron -- cell body in ganglion, axon terminal
in effector organ.
B. Sympathetic division.
1. Reaction to emergencies -- "fight or flight".
2. Effects.
a. Increased heart rate.
b. Increased blood sugar.
c. Increased blood flow to skeletal muscles.
d. Dilation of pupils.
3. Division is activated as a unit.
4. Anatomy.
a. Preganglionic neurons originate in thoracic and lumbar regions of
spinal cord.
b. Most ganglia lie near spinal cord (sympathetic chain) (fig. 6-45).
5. Neurotransmitters.
a. Preganglionic neurons release acetylcholine (ACh).
b. Postganglionic neurons release norepinephrine (NE).
c. NE binds to adrenergic receptors on effector organ.
6. Adrenal medulla is innervated by preganglionic sympathetic neurons.
a. Secretes epinephrine in response to sympathetic stimulation.
b. Effects are similar to those of NE.
C. Parasympathetic division.
1. Vegetative functions -- "rest and digest".
2. Effects are usually opposite to those of sympathetic nervous system.
a. Decreased heart rate.
b. Increased blood flow to internal organs.
c. Contraction of smooth muscle in intestinal wall.
d. Constriction of pupils.
3. Individual organs are controlled separately.
4. Anatomy.
a. Preganglionic neurons originate in brain stem and sacral spinal
cord.
b. Ganglia lie in or near effector organs.
5. Neurotransmitters.
a. Preganglionic neurons release ACh.
b. Postganglionic neurons release ACh.
c. ACh binds to cholinergic receptors on effector organs.
D. Dual innervation.
1. Most organs are innervated by both sympathetic and
parasympathetic neurons (fig. 6-44).
2. Two divisions usually produce opposite effects (table 6-11).
3. Example:
E. Summary table.
Characteristic
Sympathetic
Parasympathetic
Function
Activation
Effects on HR
Blood flow increased
Effects on pupils
Preganglionic NT
Postganglionic NT
VII. Autonomic Receptor Subtypes and Blockers (Rat Intestine Lab).
[pp. 123, 166-168, 266-267]
A. Parasympathetic Division.
1. Acetylcholine binds to cholinergic receptors.
2. Atropine.
a. Blocks cholinergic receptors -- anticholinergic.
b. Actions.
1. Pupillary dilation.
2. Dry mouth.
3. Constipation.
c. Clinical uses.
1. Antispasmodic.
2. Pre-anesthetic -- inhibits salivation.
3. Nerve gas antidote.
d. Research tool.
1. Used to identify if a physiological response or drug action
involves cholinergic receptors.
B. Sympathetic Division.
1. Epinephrine and norepinephrine bind to adrenergic receptors.
2. Adrenergic receptor subtypes (table 6-11).
a. Alpha-adrenergic receptors.
1. In walls of most arterioles, epinephrine causes smooth muscle
contraction
> constriction of arterioles>increases blood pressure.
b. Beta-adrenergic receptors.
1. Increases heart rate.
2. In walls of bronchioles, epinephrine causes smooth muscle
relaxation
> dilation of airways> improves air flow.
3. Adrenergic blocking drugs.
a. Tolazoline.
1. Alpha-adrenergic blocker -- competes with epinephrine for
alpha-receptors.
2. Relaxes arteriolar smooth muscle
>decreases blood pressure.
3. Too many side effects to be clinically useful.
b. Propranolol.
1. Beta-adrenergic blocker -- competes with epinephrine for
beta-receptors.
2. Decreases heart rate.
3. Commonly used to lower blood pressure.
4. James Black -- research in receptor subtypes.
a. Discoverer of propranolol.
c. Selective adrenergic blockers can be used to determine the
relative abundance of the two types of adrenergic receptors
in a tissue.
VIII. Effects of Neurotransmitter or Hormone Binding. [pp. 287-289]
A. Excitatory effects (ex. ACh on intestinal smooth muscle).
1. NT binds to receptor on cell membrane.
2. Opens Ca++ channels (fig. 5-5a).
3. Ca++ binds to calmodulin.
4. Contraction.
B. Inhibitory effects (ex. NE on intestinal smooth muscle).
1. NT binds to receptor on cell membrane.
2. Closes Ca++ channels.
3. Cytoplasmic Ca++ levels decline.
4. Relaxation.
C. Second messengers.
1. Cyclic AMP usually causes smooth muscle relaxation.
2. Example: Epinephrine on bronchial smooth muscle.
a. Binds to beta-adrenergic receptors on cell membrane.
b. Activates adenylyl cyclase on inner surface of membrane (fig. 5-6).
c. Causes production of cyclic AMP (second messenger).
d. Cyclic AMP initiates biochemical changes inside cell
>relaxation.
