Exam #1: Smooth Muscle Flashcards Preview

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Flashcards in Exam #1: Smooth Muscle Deck (37):

List the characteristics of smooth muscle. How does smooth muscle differ from skeletal muscle?

- Smooth muscle is composed of smaller shorter fibers than skeletal muscle
- Smooth muscle is non-striated vs. striated skeletal muscle
- Different types of smooth muscle exist (multi-unit vs. unitary) in different organs


What is the difference between multi-unit & unitary smooth muscle?

Multi-unit= discrete smooth muscle fibers that contract independently
- Each fiber is independently innervated by the ANS
- Individual fibers do NOT communicate

Unitary= Large number of fibers that contract together as a single unit
- Neuronal & non-neuronal factors regulate
- Cells communicate via gap junctions


Locations of multi-unit smooth muscle

- Ciliary & iris muscle of the eye
- Piloerector muscle


Locations of unitary smooth muscle.

- GI Tract
- Bile Ducts
- Ureters
- Uterus
- Blood vessels


What contractile component is missing from smooth muscle that is present in skeletal muscle?

Troponin Complex
- Indicative of a different role of Ca++ in smooth muscle

Smooth muscle does contain actin, myosin, and tropomyosin


How are myosin heads arranged in smooth muscle? How is this different from skeletal muscle?

Mysoin heads in smooth muscle are NOT all arranged in the same direction


What takes the place of z-discs in smooth muscle?

Dense bodies


What is the function of dense bodies?

- Transmission of force from once cell to another
- Anchor for thin filaments


What attaches to the dense body & what is between them?

Thin filaments (actin) are attached to the dense body; thick (myosin) are interspersed between the thin filaments


How are actin & myosin arranged in smooth muscle? What is the functional outcome?

Actin & myosin are arranaged in every plane, which allows fro the entire cell to contract i.e. shrink or bulge


Review the contractile events that occur in skeletal muscle, starting with the attached state.

1) Myosin attached to actin
2) Myosin binds ATP leading to detachment
3) ATP hydrolysis to ADP & Pi resets the myosin head
4) Cross-bridge forms & myosin binds a new position on actin
5) Pi is released leading to a change in position of myosin-->power stroke
6) ADP released


How does the point of regulation differ from skeletal muscle to smooth muscle?

- Smooth muscle targets myosin
- Skeletal muscle uses Ca++ to regulate actin


Outline the events of contraction in smooth muscle.

1) Increased intracellular Ca++ from extracellular space
2) Ca++ binds Calmodulin
3) Calmodulin-Ca++ binds & activates myoskin light chain kinase (MLCK)
4) MLCK phosphorylates myosin regulatory chain & allows for activation of the myosin ATPase
5) Cross bridging occurs when myosin is phosphorylated at the regulatory chain


What is different between contraction of skeletal muscle & smooth muscle?

1) In smooth muscle ECF Ca++ is the PRIMARY source of Ca++, NOT SR Ca++ as in skeletal muscle
3) Myosin ATPase is constitutively active in skeletal muscle; smooth muscle, this is regulated
4) Cross bridging occurs as long as myosin is in the phosphorylated state


Describe the events of actin-myosin cross-bridging in smooth muscle.

1) MLCK phosphorylates Myosin ATPase to turn it ON
2) Myosin- ADP+Pi is attached to actin= cross-bridge formed
3) Release Pi + ADP from myosin= power stroke
4) ATP binds myosin= release
5) ATP hydrolysis to ADP+Pi= new cross-bridge formed


What is the result of decreased MLCK activation?



What causes relaxation in smooth muscle?

1) Intracellular Ca++ decreases, preventing MLCK activation & necessary phosphorylation/ activation of Myosin ATPase
2) Dephosphorylation of myosin by myosin phosphatase


What leads to tonic contraction in smooth muscle?

Once the cross-bridge is formed, dephosphorylation of the Myosin ATPase regulatory site
- Reduced ATPase activity follows
- Very slow power stroke occurs
- Maintenance of the cross-bridge for a long time= tonic contraction


List the differences between smooth muscle & skeletal muscle in terms of contraction. Specifically address: 1) General Characteristics, 2) Cross-Bridge Cycling, 3) Energy
4) Contraction/Relaxation, 5) Maximum Force, 6) Latch Mechanism, & 7) Stress-relaxation.

- Smooth muscle can produce long tonic contractions that occurs for hours or days vs. rapid contraction & relaxation in skeletal muscle
- Slow cross-bridge cycle in smooth muscle vs. fast cycle in skeletal
- Low energy demand in smooth muscle vs. high energy demand in skeletal muscle
- Relatively long onset & duration of contraction in smooth muscle vs. fast onset, duration, & relaxation in skeletal muscle
- Higher maximum force of contraction in smooth muscle vs. skeletal muscle
- Latch can produce tonic contraction in smooth, which is not present in skeletal muscle
- Relaxation & contraction can occur in response to stretching & filling to maintain constant pressure in smooth muscle, which does not occur in skeletal muscle


How does the neural regulation of smooth muscle differ from skeletal muscle?

- No structural neuromuscular junction like in skeletal muscle
- Diffuse branches of nerves overlie smooth muscle
- Multiple varicosities along the nerve fiber instead of end feet
- Increased space between varicosity & muscle fibers


What is the difference between diffuse junctions & contact junctions in smooth muscle?

- Diffiuse junction= seen in unitary smooth muscle; nerve fiber does NOT contact the sheet of muscle
- Contact junction= seen in multi-unit smooth muscle; nerver fiber does contact the muscle fibers

Note that contact junctions resembe neuromuscular end feet seen in skeletal muscle


What are the primary neurotransmitters that regulate smooth muscle?

Acetylcholine & NE


In general, what effect will acetylcholine & NE have?

Opposite; it is difficult to tell if it will cause contraction of relaxation (tissue-dependent)


What is the effect of NO on smooth muscle?



Define electromechanical stimulation.

- Change in membrane permeability resulting in depolarization of smooth muscle

I.e. opening Na+ &/or Ca++ membrane channels leading to a depolarization


Define pharmacomechanical stimulation.

- Activation of signaling molecules that through the generation of second messengers activate the contractile process.

E.g. Hormone activates PLC, increasing IP3 & Ca++; increase of intracellular Ca++ causes contraction of smooth muscle


Define electromechanical inhibition.

- Change in membrane permeability that results in hyperpolzarization of smooth muscle

E.g. close Na+ &/or Ca++ channels or open K+ membrane channels.


Define pharmacomechanical inhibition.

- Activation of signaling molecules that through the generation of second messengers inhibit the contractile process.

E.g. Hormone activates PKA that phosphorylates MLCK, preventing Ca++-Calmodulin from binding & activating MLCK


What are the two sources of Ca++ in smooth muscle? Which is the primary source?

ECF= primary
SR= secondary


What are the two roles of Ca++ in smooth muscle?

1) Membrane depolarization i.e. influx of Ca++ & Na+ are important for action potential
2) Contraction via the activation of MLCK


What are the two types of action potentials that occur in smooth muscle?

1) Spike potentials
2) Action potentials with plateaus


Draw a spike potential & List the different ions that important for the phases the action potential.



Draw an action potential with plateau & list the different ions that important for the phases of the potential.



What are slow wave potentials?

A continuous cycling of depolarization & repolarization without eliciting a spike potential that leads to a contraction.
- Seen in some types of smooth muscle
- Serve as pacemakers for some types of smooth muscle
- An action potential could occur at the peak of the slow wave



What causes slow-wave potentials?

Na+ pumping or rhythmic changes in ion conductance


What ion is primarily responsible for depolarization during action potentials in smooth muscle?


*Note that Na+ does play a role, but Ca++ is primary, like cardiac action potentials.


What ion is responsible for the prolonged state of depolarization seen in action potentials with plateaus?


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