1-Smooth Muscle Physiology Flashcards

1
Q

development

A
  1. mesoderm
  2. endothelial intermediates
  3. mesenchymal progenitors
  4. immature smooth muscle
  5. mature smooth that aggregate but not fuse
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2
Q

organization

A

large mononucleated with non-uniform arrangement aka not striated

no z discs instead dense bodies @ cytoplasm for thin filaments or dense plaques @ cell membrane for thick
-linked to each other by intermed filaments

sarcolemma invaginations aka caveolae to inc surface area and lined with receptors instead of t tubules

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3
Q

function in GI

A

@ upper GI (esophagus and esoph sphincter) important to move food to stomach and regulate entry
@stomach is phasically active/rhythmic to mix food with gastric juices

esoph normally relaxed, sphincter normally contracted

phasically- looks like waves

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4
Q

function in blood vessels and airways

A

normally partially active to keep open/patent
-if not constantly active then airways/vessels collapse/diff to maintain blood pressure

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5
Q

electrophysiological properties

A
  1. action potential sole stimulus for force
  2. oscillations in membrane potential = gen of action potential = force
  3. oscillations in membrane potential alter force w/o action potential
  4. hormones or duge alter force indep of membrane potential

basically diverse- force from membrane pot with or without AP

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6
Q

myogenic response

A

mechano-dependent response in small A’s and arterioles in cerebral, mesentaric, cardiac, renal beds aka autoregulation blood flow when BP changes

-inc transmural pressure> vessel diameter inc >stretch sensitive ion channels open > inc intracell Ca > vascular smooth contracts to dec blood vessel diameter

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7
Q

myogenic response

A

mechano-dependent response in small A’s and arterioles in cerebral, mesentaric, cardiac, renal beds aka autoregulation blood flow

-inc transmural pressure> vessel diameter inc >stretch sensitive ion channels open > inc intracell Ca > vascular smooth contracts to dec blood vessel diameter

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8
Q

innervation

general

A

no motor end plate so instead varicosities release neurotransmitter to diffuse across diffuse junction

varicosities look like beads

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9
Q

methods of contraction

A
  1. single unit- contract in unison due to abundance of gap junctions to permit transmission of depolarization/Ca ions
    -GI and urogenital tract
  2. multiunit- contraction dependent on local neurotrans release
    -airways and vasculature
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10
Q

dual innervation GI

A

multi converging inputs to control activity
1. intrinsic- enteric system in lining of tract to sense mechanical/chem conditions and control motility via cells of cajal (ICC)
2. autonomic- para/sympathetics to alter motility by regulating ICC

ICC has intrinsic pacemaker activity for rhythmic contractions,

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11
Q

contraction steps

A
  1. Ca influx into cytoplasm
  2. activation of calmodulin (Ca binding protein)
  3. CaM activates myosin light chain kinase MLCK
  4. MLCK phosphorylates regulatory light chain on myosin neck (thick fila)
  5. cross bridge cycle
  6. free Ca pumped out or sequestered in SR
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12
Q

myosin light chain phosphatase

A

MLCP reverses MLCK by removing phosphate from myosin

consititutively active but modulated by hormones/neurotrans

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13
Q

cross bridge cycle

A
  1. phosphorylation of light chain changes conformation so myosin head bind actin
  2. ADP and Pi are lost
  3. power stroke
  4. new ATP binds myosin head so detach from actin
  5. ATP hydrolyzed and head cocked position to repeat cycle
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14
Q

excitation stimuli

A

multi stimuli
1. neurotrans from nerve cells in close proximity (neural)
2. circulating hormones (endocrine)
3. substances from nearby cells (paracrine)

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15
Q

ways to initiate excitation

extracellular

A
  1. voltage Ca channels LTCC, need depolarization
  2. receptor mediated- need ligand

both result in conformational change for extracell Ca to flow in

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16
Q

excitation

intracellular

A
  1. ligan binds g protein coupled receptor
  2. IP3 released
  3. IP3 binds its receptor on membrane of SR
  4. conform change
  5. release Ca from SR

Ca from SR can modulate membrane potential so facilitate influx of Ca by depolarizae or hyperpolar

17
Q

other G receptor regulation

A

Gs = activate adenylate cyclase to inc cAMP > inc PKA
PKA phosphorylates MLCK to inhibit and dec contraction

Gi will inhibit adenylate cyclase

Gq binds acetylcholine to release IP3 and inc Ca, maintain tension in airway

18
Q

clinical presentation smooth muscle defects

A
  1. regulation of blood pressure/flow
  2. urinary continence
  3. vision
  4. airway caliber
  5. GI motility
  6. pregnancy/labor
19
Q

hypertension

A

angiotensin receptor blockers used to treat high BP to prevent G protein receptors to dec intracell Ca

Ca channel blockers too but not affect skeletal muscle bc dependent on Ca released from SR

20
Q

asthma

A

acc of cellular debris from epithelial damage and airway inflamm = submucosal thick by edema

muscle contraction, hyperplasia, hypertrophy

21
Q

beta2-adrenergic agonists

A

attenuate smooth contraction via cAMP/PKA mechanisms
1. phos and activate K channels
2. phos and inhibit G receptor IP3 pathway
3. phos and activate Na/Ca exchanger and Ca/ATPase
4. phos and inhib myosin light chain kinase

aka dec bronchoconstriction during aggravation of asthma but deleterious if long term

use anti-inflamm for long term treat