Smooth Muscle Flashcards
Where are the smooth (S) mm found?
although the variety and function of S mm is amazing. It mostly surrounds hollow organs (blood vessels, bronchi, gut, reproductive and urinary tracts) and are arranged in sheets
What are some of the functions of S mm?
Maintains pressure-circular layer in airways, blood vessels
Mix and Propel contents-circular and longitudinal layers in intestinal wall
Regulates internal flow-rectangular layer in bladder, rectum, small testicular duct
In terms of contractile elements, what are the 2 structures missing in S mm but present in C mm, and SK mm?
Troponin- instead they have Calponin and Caldesmon
T-Tubules
What are other unique characteristics of S mm?
- Have calponin and caldesmon instead of troponin
- Lack T-tubule
- contain less developed SR
- Dense areas (points of mechanical coupling) analogs to Z lines in striated mm
- Gap junction (points of electrical coupling)
- Thick and thin filaments organized diagonally
Where does Ca need for contraction come from?
Ca needed for contraction come from the extracellular space and SR unlike in SK mm where it solely comes from SR.
What is the difference b/n tonic and phasic contraction?
Tonic: maintain a continuous level of partial contraction (tone). Ex: walls of blood vessels, airways of the lungs, sphincters. NO AP needed to initiate contraction but affected by Em, not at elevated Ca, sustained stimulation
Phasic: contract rhythmically or intermittently in GI, reproductive, and urinary systems. NEED AP to initiate contraction, short stimulation
Label and understand Tonic and Phasic contraction figures.
pp. 6
T/F Unlike in cardiac mm, S mm need extracellular Ca for contraction.
F. Both need extracellular Ca influx that causes CICR from SR. But S mm also uses the release of IP3.
How does IP3 result in cytoplasmic [Ca] increase?
- Agonist bind to Ca channels and activate a pathway that results in IP3 release.
- IP3 goes to SR to stimulate IP3 R
- Ca released from SR
Label/Study Sources of Ca for S mm contraction Figure
pp7
If S mm lack troponin, how does Ca control contraction in S mm?
Ca bind to calmodulin-Ca-calmodulin complex activates myosin light chain kinase (MLCK)-MLCK hydrolyzes ATP to phosphorylate inactive myosin-trigger crossbridge formation (Figure on pp. 8).
What is the Ca switch that turns on the contractile apparatus in S mm, and striated mm?
S mm: Ca dependent phosphorylation of MLC
Striated (C mm and SK mm): Ca binding to troponin
What is the rate-limiting step in S mm contraction?
Phosphorylation of the myosin head. Unlike SK mm, in S mm regulation of cross-bridge occurs on the thick filament.
Understand Figure showing rate limiting step.
pp. 9
T/F Myosin ATPase of S mm splits ATP at a much slower rate than SK mm.
T. S mm can generate more tension per unit of cross sectional area (Figure pp 10).
What induces S mm relaxation?
- NO-PKG- inactivate MLCK
- Epinephrine-PKA-inctivate MLCK
- Myosin light chain phosphatase-dephosphorylate myosin head.
Some types of S mm cells are self excitable (in the absence of hormonal and neural input). What are the processes they use for spontaneous excitation?
Pacemaker Potentials: spontaneous depolarization due to cationic current (mostly Na coming in)
Slow-wave Potentials: spontaneous hyperpolarizing and depolarizing swings (electrogenic pumps activity)
The contractile activity of S mm can be controlled by numerous factors such as _____, _____, ______, and ______
- Electrical Activity
- Hormones
- Autonomic Nerves
- Drugs
T/F Summation and tetanus take place in SK but not in S mm and C mm.
F. Summation and tetanus happen both in SK and S mm but not C mm.
S mm cells produce a wide range of membrane potential (Vm) variations that can either initiate or modulate contraction. Mention 4 of these variations:
- AP: twich, summation (E-C coupling)
- Slow-waves with AP bursts at waves crests (E-C coupling)
- Changes in Vm: chronic hyperpolarization and depolarization (E-C coupling with no AP)
- Contractile activity with no changes in Vm: chemical influence (drugs and hormones) (Pharmaco-mechanical coupling).
How does the ANS synapse on S mm cells differ from neuromuscular junction?
The postganglionic autonomic fibers travel across the surface of S mm cells. The varicosities will release neurotransmitter that will travel to neighboring S mm cells with adrenergic and cholinergic receptors. More wide spread and slow propagation of neurotransmitters.
NOTE: transmitter release modify rate and strength of activity.
What are the two types of S mm based on electrical characteristics of their plasma membrane?
1) Multi-Unit
2) Single Unit
What cells resemble Multi-unit and single-unit S mm?
Study Figure pp19
1) Multi-Unit- resemble SK mm b/c no electrical coupling (lack gap junction), & neuronal regulation is important.
2) Single-unit-resemble C mm b/c electrical activity is propagated via gap junctions
Mention some of the hormones and neurotransmitters that modulate the S mm?
-Adrenergic agents (usually induce contraction)
B2-Adrenergic receptor: coupled to Gs ptn, increases adenylate cyclase, increases cAMP, increases PKA
-Respiratiory: dilation of bronchial S mm open airways
-GI: decrease ,motility of S mm (decrease peristalsis)
Alpha 2 Adrenergic receptor: coupled to Gi ptn, decrease adenylate cyclase, decrese cAMP, decrease PKA
-OPPOSIT OF B2 effects
Alpha 1 Adrenergic receptor: coupled to Gq ptn, PLC-IP3-mediated Ca signaling -CV: peripheral vasoconstriction
- ACh (Muscaranic receptors: cause most to contract but some to relax)
- Eye-contraction of the pupil
- CV-vasodilation of coronary blood vessels
- Respiratory: constriction of bronchial S mm narrow airways
- GI: increase motility
- Renal: contraction of the bladder.
What are some hormones, drugs and local metabolites that affect S mm? Study Figure pp 22
- hormones (histamine, serotonin, vasopressin, oxytocin, angiotensin, gastric hormones)
- Mechanical stretch (opens mechano sensitive channels leading to depolarization)
- Local metabolites (CO2, lactic acid)
- Drugs: Ca antagonists, K channel blockers, NO/cGMP stimulators
