Exam 3 Skeletal and Smooth Muscle Contraction Flashcards

1
Q

Sarcoplasmic resticulum, t-tubules (triads), Locations

A

A-I junction in fast twitch muscle (2 triads per sarcomere - fast twitch, A-I junction)
Z-line in slow twitch muscle, 1 triad per sarcomere - Slow twitch, (z-line)

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2
Q

Function of t-tubules

A

spreads AP to inner portion of muscle fibers

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3
Q

Function of sarcoplasmic reticulum

A

storage site for calcium, calcium is release from SR following depolarization of muscle cell

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4
Q

Sliding filament theory

A

muscle contraction results from actin filaments “sliding” over myosin; myosin “pulls” actin fibers towards the m-zone (mid point of sarcomere); myosin/actin movement draws z-lines together, causes shortening of the sarcomere, the myofibrils and the muscle fiber; action occurs throughout all of the sarcomeres of the depolarized muscle fiber

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5
Q

lever arm hypothesis

A

myosin heads extend to contact the thin filaments forming cross bridges (after Calcium binds TnC), globular hears from each myosin filament contact several (6) surrounding actin proteins; once a cross bridge forms, the head/neck of myosin bends toward the sarcomere center (power stroke) causing actin to slide over myosin; actin filament moves over thick filament (moves a distance of ~5-15 nm)

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6
Q

Energetics of sliding filament theory

A

(1) A cycle of muscle contraction is described to begin with ATP binding to myosin head, binding induces dissociation of cross bridge from actin; ATP binding to myosin is followed by ATP hydrolysis by ATPase of myosin heads (ADP and Pi stay bound to myosin, energy released is absorbed by myosin, myosin head is now an energized state, prepared to perform the power stroke)
(2) Muscle cell is depolarized due to AP from motorneuron; depolarization reach SR (triad) and stimulates the release of calcium from the SR; Calcium binds troponin-C, which causes tropomyosin to “uncover” actin binding sites; energized myosin attaches to actin binding sites; myosin pulls actin toward center of sarcomere = power stroke
(3) Following the power stroke, ADP and Pi dissociate from myosin; new ATP attaches to myosin head to cause release of cross-bridge and rocking of myosin head (myosin is reset via hydrolysis of ATP into ADP and Pi, this returns myosin in the energize state); myosin stays in energized state until a new signal for muscle contraction is received from motorneuron

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7
Q

Sequence of Skeletal muscle Contraction

A
  • Motoneuron propagates action potential
  • ACh (in Vesicles of motoneuron) is released into synaptic trough containing subneural clefts
  • ACh binds to its nicotinic receptor (binding opens channels to allow influx of sodium into muscle cell)
  • Sodium influx depolarizes the muscle cell which generates an AP in the muscle cell (sarcolemma)
  • T-tubules propagate AP to interior of muscle cell to the triads (t-tubule and 2 SR cisterns)
  • AP depolarization of T-tubule activates SR membrane and stimulates opening of Calcium channels of the SR
  • Calcium floods into the sarcoplasm and binds to troponin-C molecules on the thin filament
  • Calcium binding causes conformational change in troponin-T which causes tropomyosin to move and expose binding sites on actin proteins
  • energized myosin head binds with the binding sites on action forming cross-bridges
  • myosin pulls on actin filaments to shorten the sarcomere -sliding filament (power stroke)
  • Calcium is quickly pumped back into SR (need another AP in muscle cell to stimulate another calcium surge)
  • If APs are continually received from motorneuron, enough calcium remains in sarcoplasm to allow sustains fiber contraction - tetany
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8
Q

Relaxation after contraction

A
  • motoneuron action potentials cease
  • dissociation of calcium from troponin-C
  • Calcium actively pumped back into sarcoplasmic reticulum
  • sarcomere returns to resting position
  • myosin head binds ATP and hydrolyzes it into ADP and Pi, and is ready for the next calcium surge
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9
Q

Smooth muscle morphology

A

smooth muscle cells are much smaller, contain fewer thick and thin filaments (in comparison to skeletal muscle cells); cells are connected by gap junctions which affords easy cell-to-cell transmission of electrical potentials

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10
Q

two major types of smooth muscle

A

multi-unit (present in optic muscles)

Unitary (present in abdominal viscera and most blood vessels)

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11
Q

Characteristics of mutiunit smooth muscle

A

composed of discrete, separate muscle fibers (cells); each muscle fiber acts independently; fibers are held together by CT

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12
Q

Locations of multi unit smooth muscle

A

ciliary muscle and iris muscle of the eye; piloerector muscles of hair follicles

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13
Q

Locations of unitary (visceral or syncytial smooth muscle)

A

GI tract, bile ducts, ureters, uterus, blood vessels

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14
Q

Characteristics of unitary smooth muscle

A

muscle fibers are arranged in sheets or bundles and contract together; cell membrane of each muscle fiber is in contact with neighboring cells at multiple sites (gap junctions allow for spread of APs, thus fibers can contract in unison)

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15
Q

Thin filament (actin-calmodulin) structure of Smooth muscle

A

Filamentous network of globular actin units (similar conformation of actin filament as in skeletal muscle); actin filaments are bound to calmodulin to make the thin filament (no tropomyosin or troponin as in skeletal muscle); thin filaments are anchored to the cell membrane at “dense bodies” (dense bodies are analogous to z-discs of sk. muscle)

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16
Q

Thick filament (myosin) structure of smooth muscle

A

polymerized heavy chains and light chains with globular heads as in sk. muscle; thick filaments overlap with actin filaments similar to sk. muscle; there is no defined sarcomere structure of thin and thick filaments

17
Q

Dense bodies

A

complex of intermediate protein filaments that are attached to cell membrane proteins; serve as anchorage sites for thin (actin) filaments; also muscle cells are bound together at the dense bodies (binding allows force transmission from cell to cell); arrangement of myosin heads and intermediate filament proteins allows for smooth muscle cells to shorten down to 20% of original length (Sk. muscle fibers shorten to 60-70% of original length)

18
Q

Smooth muscle NMJ

A

C-motoneuron (from autonomic nervous system) for a diffuse network of varicosities at axon terminals (varicosities contain neurotransmitter, no specific one-to-one NMJ); AP from C-motorneuron causes release of NTs, NTs are released into the area around muscle cells, and diffuse toward muscle cell receptors; axon terminals contact only outer layer of smooth muscle fibers (AP is propagated to interior cells via gap junctions)

19
Q

Smooth muscle contraction

A

-stimulus for contraction (AP) initiates calcium ion influx into muscle fiber to create depolarization
-Calcium serves to depolarize the muscle fiber
THEN
-Ca binds to calmodulin
-Calmodulin-calcium complex initiates enzymatic phophorylation of myosin head, (addition of ATP to myosin; ATP remains attached to myosin as long as intracellular calcium remains high - e.g. NTs are continually released)
-Myosin completes cross-bridging and contraction on action repetitively (as long as ATP is attached)
-Calcium pump removed Ca from cytosol (when stimulus from motorneuron ceases)
-Pump operatres continuously, but it operates slowly
-Longer period to re-establish RMP following depolarization
-Repolarization of muscle cell stimulates enzymatic removal of ATP from myosin and contraction stops (myosin phosphatase)

20
Q

Stimuli for Smooth muscle contraction

A

Autonomic nerve fibers that release ACh or Norepinephrine as NTs (depending on location of muscle fiber and type of receptor, NT can cause either contraction of relaxation)

  • Stretch of muscle cells (e.g. GI tract) creates depolarization and contraction
  • Spontaneous depolarization and resulting contraction (rhythmical contraction of gut muscle)
21
Q

Hormones effect on smooth muscle activation

A

Affect both excitation and inhibition through numerous hormones and receptors

22
Q

Stimuli for smooth muscle relaxation (local tissue factors0

A
  • hypoxia - causes smooth muscle relaxation and thus vasodilation or vasculature
  • excess CO2 - causes vasodilation = smooth muscle relaxation
  • increased Hydrogen ion concentration (Acidity) causes vasodilation (Lactic acid in exercising muscle)
  • Body temp increase - causes vasodilation
23
Q

Smooth vs skeletal muscle contraction

A
  • very slow cross-bridge cycle in smooth muscle (slower opening of voltage gated Calcium channels compared to sodium channels in sk. muscle)
  • Less energy (ATP) required for smooth muscle contraction
  • Slower onset and prolonged contractions in smooth muscle
  • Maximum contraction force is great in smooth muscle (myosin-actin attachments last longer)
  • few mitochondria in smooth muscle cells (energy efficient)