Smooth muscle physio Flashcards

1
Q

connexons in smooth muscle

A

Formed like connexins in cardiac muscle, to form electrical syncytium; 1.5nm in diameter, six subunits

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2
Q

two types of smooth muscle contractions

A

tonic and phasic; tonic is constant, phasic is more like waveform. Phasic is single unit and tonic is more typically multi-unit

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3
Q

Varicosities in smooth muscle

A

varicosities are more important in the multi-unit type as each individual muscle cell has to be innervated, whereas for the single unit type of smooth muscle, the gap junctions can propagate an AP contraction (or relaxation) wave

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4
Q

examples of phasic smooth muscle

A
think GI and GU, except the vas deferens (which is already isolated because it is activated by the sympathetic system); 
GI tract
urinary bladder
ureter
uterus
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5
Q

examples of tonic smooth muscle

A
think muscles that contract for effect; sympathetic type innervations; 
pilomotor
ciliary
iris
arterioles
vas deferens
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6
Q

channels in smooth muscle

A

Present: Na/K pump
Ca pump
Ca channel (L-type)
K channel (Kv)

Notably Absent:
Na(v) - voltage gated sodium channel
T-tubules (not a channel, but important for the spread of action potentials throughout the cell)

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7
Q

messengers embedded in the sarcoplasma of smoooth muscle cells

A

IP3, DAG, cAMP (adenylyl cyclase)

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8
Q

sarcoplasmic reticulum in smooth muscle cells

A

located near the sarcolemma
contains Ca release channels that are activated by IP3
has lower capacity than the same in heart or skeletal muscle

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9
Q

tension/relaxation of smooth muscle and concordinant calcium flux

A

Ca can enter the smooth muscle cell via VGCC and ligand gated Ca channels;
It can then be released from the SR by IP3 mediated channels
These steps lead to contraction
Ca flows back into the SR or out of the cell
That leads to relaxation
p.298

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10
Q

actin/myosin/tropomyosin in smooth muscle

A

actin and tropomyosin found in greater quantities relative to myosin, compared to skeletal and cardiac muscle
not organized into sarcomeres - more like a spiral conduit with long actin filaments bound to much smaller myosin bands; all bound to dense bodies which is the midpoint of the actin filaments and the equivalent of z-discs
p. 298

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11
Q

three types of membrane depolarizations in smooth muscle

A

1) action potentials - just like skeletal or cardiac depol.
2) Rhythmical activity - wave-like potential changes that may generate quick bursts of action potentials then recede for some time
3) Graded changes in membrane potential that may be strong enough to increase contractile force
p. 299

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12
Q

action potentials in smooth muscle

A

generated by VGCC (L-type) and therefore arise much more slowly than Na gated channels

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13
Q

Rhythmical electrical activity in smooth muscle

A

produced by changes in the Ca-dependent K channels (K-sub-Ca)
p.299

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14
Q

Graded changes in electrical potential of smooth muscle

A

ligand created changes that alter K permeability. K channels are shut off by activation of PLC by DAG by Gq. depolarization (due to K maintenance) causes opening of Ca channels (L-type) which gives enough influx to cause some contraction

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15
Q

Biochemical coupling of contraction in smooth muscle cells

A

Ca can be released via IP3 by PLC (on PIP2) by Gq by alpha GPCR by norepinephrine - no action potential or membrane depolarization necessary

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16
Q

Relative contribution of intracellular Ca in smooth muscle cells during a contraction

A

usually, much more Ca comes from SR than from extra-cellular

17
Q

Smooth muscle ATP-ase is dependent on…

A

calmodulin and MLCK; calmodulin +p MLCK which +p MLC (regulatory light chain)
MLCP -p MLC to stop contraction

18
Q

DAG’s effect on smooth muscle contraction

A

DAG (from PIP2 by PLC by Gq by GPCR by alpha adrenergics (norepinephrine)) causes activation of protein kinase C (PKC) which +p CPI-17 which inhibits MLCP (causing more contraction)

takeaway = DAG - causes contraction to be prolonged

p.302-303

19
Q

RhoA’s effect on smooth muscle contraction

A

RhoA (from GPCR by alpha adrenergics (NE/Epi)) activates Rho kinase which +p MYPT1 (targeting subunit of MLCP) inhibiting it

takeaway - RhoA causes contraciton of smooth muscle to be prolonged

clinically: RhoA overexpression is linked to hypertension and arterial vasospasms
p. 302-303