Term
| Explain why Norepinephrine exerts different effects in vascular smooth muscle and in airway ad intestinal smooth muscle cells? |
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Definition
Different populations of adrenergic receptors in each tissue.
Vascular- Contraction
Airway and Intestine- Relaxation |
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Term
| Explain the differences in gross and contractile structure between striated and smooth muscle cells. |
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Definition
Smooth
- less structured and irregular arrangement of filaments
- Variable length of actin and myosin filaments
- Actin filaments attach to dense bodies in cytoplasm and lie in parallel with myosin fibers
Striated
- Highly structured sarcomere
- Consistent filament length
- More elaborate sarcoplasmic reticulum |
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Term
| How is contractile activity achieved in smooth muscle cells? |
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Definition
Players- actin, myosin, calmodulin
1) Calcium binds calmodulin, which activates MLCK
2) MLCK phosphorylates 1 light chain on each myosin head (takes Pi from ATP) and enables it to bind to actin (ESSENTIAL STEP)
3) at low Ca concentrations, Myosin phosphatase removes the Pi and deactivates contraction. |
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Term
| Why is myosin invisible in EM sections of resting smooth muscle? |
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Definition
Unphosphorylated MLC assume folded state where myosin precursor proteins (light meromyosins) cannot associate to form filaments.
Phosphorylation-induced unfolding exposes actin biniding sties AND allows aggregation of myosin filaments
(MLCK is also present in skeletal muscle, but not required for function). |
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Term
| What do "latch bridges" have to do with the much longer contractile times exhibited by smooth muscles relative to skeletal muscles? |
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Definition
Short- ATP-independent, lasting contractions!
"Latch Bridges" are formed when myosin phosphatase dephosphorylates the MLC while the cross-bridge is still attached to actin.
If this occurs, muscles will remain in tension without requiring more ATP. This allows smooth muscles such as vascular smooth muscle to remain tonically active without being metabolically demanding (same ATP generates 2 minutes of smooth muscle activity compared to 3 seconds of skeletal muscle activity). |
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Term
| How is the nervous system supply different in Unitary (visceral) smooth muscle than in Multiunit smooth muscle? |
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Definition
1) Unitary (visceral) in the GI and Uterus have
- high degree of spontaneous activity in the absence of direct innervation due to GAP JUNCTIONS
-fibers innervate only outer layer and excitation travels inwards (slow excitation/contraction link)
- Pacemaker cells fire at intrinsic rhythms and have unstable membrane potentials
2) Multiunit smooth muscle cells of the vas deferens, ciliary bod of the eye and pilomotor muscles have
- very little spontaneous activity (no Gap Junctions)
- innervation is much closer to target cell (quicker excitation/contraction link)
- each muscle cell makes contact with a nerve ending
- similar regulation to skeletal muscle |
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Term
1) What are "slow waves"?
2) Where/how are they generated? |
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Definition
1) Spontaneous activity resulting from fluctuations of membrane potential in "pacemaker" smooth muscle cells.
2) Interstitial cells of Cajal
Fluctuations in K+ conductance
Na+/K+ pump |
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Term
| How does "stretch activation" occur in skeletal vs. smooth muscle? |
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Definition
1) Skeletal- "muscle spindle" detects stretch and fires, eliciting spinal chord reflex and postural muscle contraction.
2) When hollow organs stretch, mechano-gated Calcium channels open and cells fire. |
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Term
| Explain the difference between "tonus" in smooth muscle and "tetany" in skeletal muscle. |
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Definition
Fast:
SmM contraction length and strength depend on firing rate and resulting intracellular calcium concentration (Tonus)
SkM contraction generates a maximal level of activation from a single twitch (Tetany)
Explanation:
Recall, smooth muscle contraction is Na-independent, and relies only on Voltage-gated calcium channels (electrochemical gradient). Thus Ca serves as a current carrier AND the molecule that links excitation/contraction
Contraction varies as a function of action potential frequency AND resultant graded increases in intracelllar calcium. |
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Term
| How can smooth muscle contraction be initiated without action potential generation? |
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Definition
1) Local chemical factors such as low O2, high CO2 and low pH in interstitial fluid
In vascular smooth muscle (precapillary sphincters), these factors can cause local dilation even with high sympathetic tone (feedback mechanism).
This mechanism occurs either through K+ channel opening and hyperpolarization or direct Ca-inhibition.
2) Hormone-induced contraction through membrane bound-receptors in vascular and pulmonary systems (pharmomechanical coupling).
Calcium enters through receptor-operated channels (ROCs).
Example- activation of IP3 through alpha-adrenergic receptor inhibits action potential generation though Ca-activated K-channels that hyperpolarize the membrane potential. Contraction is therefore controlled by hormone-regulated calcium influx. |
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Term
| How can contraction in certain muscle cells (GI smooth muscle, uterus, ureter) be hormone-regulated instead of action-potential-regulated, when voltage-gated calcium channels are still present? |
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Definition
Activation of IP3 through alpha-adrenergic receptors inhibits action potential generation though Ca-activated K-channels that hyperpolarize the membrane potential.
Contraction is therefore controlled by hormone-regulated calcium influx, and not action potentials. |
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Term
| Why might faster contracting smooth muscles such as pilorector muscles have more caveolae than slow contracting smooth muscle cells? |
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Definition
sarcoplasmic reticulum tubules are localized to membrane invaginations called caveolae.
Calcium entry through membrane is slower than internal calcium release, so when you want a "fast contraction," you want to use internal release. |
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Term
| How is smooth muscle relaxation achieved (how is calcium concentration kept low in the cell)? |
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Definition
1) Slow acting pump puts calcium in SR or extracellular path (slow speed accounts for longer contraction)
2)BAR-cAMP-Na/K pump- Na/Ca exchanger
B-adrenergic receptor activation leads to increased cAMP, which activates the Na/K pump, which provides the proton-motive force for the Na-Ca exchanger.
cAMP increases also reduce affinity of MLCK for its phosphorylase and blocks IP3 production. |
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Term
| Why do you find axon varicosities in smooth muscle cells? |
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Definition
Nerve fibers in smooth muscle course for long distances b/w adjacent muscle fibers (no NMJ). Varicosities are bulging regions where neurotransmitters are released (they are nerve-muscle contact points where Schwanna cell coating is interrupted and neurotransmitters can diffuse out).
They are more commonly found close to target muscles in multi-unit smooth muscle, where excitation/contraction is more tightly linked. |
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