Smooth Muscle Contraction Flashcards

1
Q

what is the organization of contractile proteins in smooth muscle?

A

has thick myosin and thin actin filaments that are not organized into sarcomeres. the thin filaments are anchored to dense bodies

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2
Q

describe the contraction of smooth muscle.

A

it is slow in contraction and relaxation but it shortens very much

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3
Q

do smooth muscle cells contain T tubules? what is the organization of the sarcolemma?

A

there are no t tubules

the sarcolemma contains calveolae- microdomains that have many cell receptors and ion channels

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4
Q

what types of receptors and channels are contained within the calveiolae of smooth muscle cells?

A

muscarinic ACh receptors and adrenergic receptors

L-type Ca channels, ATP sensitive K channels, and Ca sensitive K channels

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5
Q

what relationships in smooth muscle are similar to those of striated muscle?

A

temporal relationship of action potential and the concentration of Ca and its relationship to tension

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6
Q

what is a tonic contraction?

A

a prolonged conraction with slower cross bridge cycling and a longer time spent in the tension generating phase of the cross bridge cycle

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7
Q

what is the result of a longer tension generating phase of the cross bridge cycle?

A

greater force of contraction with less energy expenditure

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8
Q

what is the reduction of length in a contracting smooth muscle?

A

up to 1/3 of original length

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9
Q

what is multiunit orgainization? does this lead to spontaneous contraction?

A

composed of discrete smooth muscle fibers innervated by a single nerve ending.
seldom spontaneous contraction

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10
Q

what is unitary organization of smooth muscle fibers? what kind of cell could this be called?

A

a sheet of smooth muscle connected by gap junctions -contract as a single unit
syncytium

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11
Q

how is unitary smooth muscle innervated?

A

little innervation because action potentials spread from cell to cell

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12
Q

which type of smooth muscle responds to stretch?

A

unitary smooth muscle

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13
Q

what controls the contraction of unitary and multiunit smooth muscle? what are some examples?

A

unitary- local factors (aiway muscle, eilliary muscle of eye, piloerector muscle)
multiunit- neural factors (small vessels, GI tract, uterus and most arteriolar muscle)

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14
Q

what calcium sources do smooth muscle use for contraction?

A

extracellular fluid

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15
Q

what are the three pathways of initiation of calcium influx?

A

L-type Ca channels activated by depolarization
G-protein coupled receptors
Ca induced Ca release from SR

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16
Q

what pathways do G coupled receptors use to cause the influx of calcium into the cell?

A

they activate phospholipase C->generates inositol triphosphate (IP3)->IP3 induced calcium release from the SR

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17
Q

what is an effective way to reduce contractile activity in both smooth and cardiac muscle?

A

L-type Ca channel blocking drugs

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18
Q

what are the two mechanisms of calcium reuptake after contraction?

A

Ca pumps in the sarcolemma and SR

3Na/Ca exchange across the sarcolemma

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19
Q

what is capacitive calcium entry?

A

the SR is refilled by calcium from outside the cell

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20
Q

how does Ca induce muscle contraction in smooth muscle?

A

Ca binds to calmodulin on myosin light chain kinase. this phosphorylates the regulatory myosin light chain and activates it

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21
Q

how does smooth muscle relax?

A

MLCP (phosphatase) dephosphorylates the regulatory light chain and blocks interaction between myosin and actin

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22
Q

what are the two categories of smooth muscle contraction? what do they have in common?

A

electromechanical and pharmacomechanical

both increase intracellular Ca-> activate MLCK and myosin

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23
Q

what is electromechanical contraction of smooth muscle?

A

opening of Ca channels in response to stretch or depolarization

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24
Q

what is pharmacomechanical contraction of smooth muscle?

A

ligand binding to cell surface receptor initiating a metabotropic response. this generates IP3 which opens Ca channels in the SR

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25
Q

can smooth muscle contractile activity be spontaneous? if so in what conditions?

A

yes- in peristaltic waves of the GI tract and in uterine contractions of labor

26
Q

what type of smooth muscle does not usually spontaneously contract and what does it respond to?

A

vascular smooth muscle

contracts in response to stretch, adrenergic neurons, endothelial cells or circulating chemical factors

27
Q

what is the resting potential of smooth muscle?

A

-50- -60 mV

28
Q

how do smooth muscle action potentials compare to contraction time? what initiates superimposed spike potentials in some visceral smooth muscle?

A

spike action potentials- much shorter relative to contraction time
slow waves- pacemaker waves

29
Q

in smooth muscle cells, what causes depolarization and repolarization of the action potential? what ion is not included in the action potential current?

A

depolarization- Ca
repolarization- K
Na not involved

30
Q

what is a basal electric rhythm? what do they dictate?

A

waves of rhythmic depolarization of intestinal smooth muscle cells (pacemaker potentials)
determine frequency, propagation velocity and direction of contractions

31
Q

what must be added to the BER to initiate action potentials?

A

must be a release of stimulatory neurotransmitters from nerves to increase the depolarization above threshold

32
Q

where does the BER rhythm change speed?

A

it changes speed in different intestinal segments depending, mostly, on size (slower in the stomach and faster in duodenum)

33
Q

what extra step is included in the smooth muscle crossbridge cycle?

A

the latch bridge state
occurs when the Ca concentration in the sarcoplasm fall and the myosin regulatory light chain is dephosphorylated while the head is still bound to actin

34
Q

why is the latch bridge state important?

A

the cell may need to maintain tension when intracellular Ca decreases

35
Q

why is the latch state maintained under dephosphorylation of the RLC? what happens if the myosin is not attached at this time?

A

because dissociation of myosin when it is dephosphorylated is very slow
if the myosin is not already attached it will remain inactive

36
Q

what is endothelin and where is it produced?

A

endothelin is a peptide produced by vascular endothelium

37
Q

what activates endothelin from its precursor? what 6 things is this stimulated by?

A

ET-1 is cleaved by endothelin converting enzyme

stimulated by angiotensin II, antidiuretic hormone, thrombin, cytokines, ROS and shearing forces

38
Q

what two effects does endothelin have on metabolic processes?

A

activates NO production

activates ETa and ETb which phosphorylates Gq-> creates IP3

39
Q

what effect does NO have on the smooth muscle cell?

A

increases cGMP decreasing contraction and increasing relaxation

40
Q

what effect does IP3 have on the smooth muscle cell?

A

causes calcium release by the SR and therefore smooth muscle contraction

41
Q

what is the general effect of endothelin on surrounding vasculature?

A

transient vasodilation and hypotension followed by prolonged vasoconstriction and hypertension

42
Q

how does endothelin related to heart pathology?

A

it is released by failing myocardium where it can contribute to calcium overolad and hypertrophy

43
Q

how does epinephrine stimulate vasodilation in some vasculature and vasoconstriction in others?

A

the vessels that contract contain alpha 1 receptors and those that dilate have beta 2 receptors

44
Q

how does epinephrine cause vasoconstriction?

A

a1 receptors activate Gq which makes IP3

IP3 causes the release of Ca and contraction

45
Q

how does epinephrine cause vasodilation?

A

b2 receptors activate Gs which stimulates the production of cAMP. This activates protein kinase A which phosphorylates MLCK and inactivates it (prevents myosin phosphorylation and contraction)

46
Q

Epinephrine stimulates vasoconstriction and dilation to which areas?

A

vasoconstriction- skin and gut arterioles

vasodilation- skeletal and heart arterioles and bronchiloar smooth muscle

47
Q

how is acute control of local blood flow accomplished?

A

by rapid changes in local vasodilation of arterioles and precapillary sphincters

48
Q

what causes the increase of blood flow through the tissues?

A

when availability of oxygen to the tissues decreases

49
Q

what is hyperemia?

A

when the rate of blood flow through the tissue increases

50
Q

what is the oxygen lack theory?

A

that low oxygen causes smooth muscle relaxation of the sphincter supplying that area

51
Q

what is the vasodilator theory?

A

that substances are released by active muscle to cause the relaxation of the sphincter (adenosine)

52
Q

what is an important local vasodilator?

A

adenosine

53
Q

what kind of receptors receive adenosine?

A

A2 adenosine receptor: g coupled receptors

54
Q

how does adenosine cause relaxation of sphincters?

A

Gs is activated by adenosine to stimulate adenylyl cyclase to produce cAMP->active PKA-> inhibit MLCK

55
Q

what is another theory of relaxation methods of adenosine?

A

A1 adenosine receptor: couples to ATP sensitive K+ channels-> hyperpolarization and decrease of Ca influx, relaxing the muscle

56
Q

what is stress relaxation?

A

a property of smooth muscle
when there is a sudden increase in volume inside the vessel, pressure will increase and then decrease slowly isovolumetrically

57
Q

what is receptive relaxation and what does it apply to?

A

the ability of smooth muscle to relax as the volume increases. important in the GI tract

58
Q

what reflexes are triggered by stomach stretching?

A

vago-vasal and intrinsic reflexes

59
Q

what is the pathway of NO production in smooth muscle relaxation?

A

ACh binds to the muscarinic receptor and stimulates Gq. this increases IP3 and the production of nitric oxide which relaxes the smooth muscle

60
Q

what is the effect of vasoactive intestinal polypeptide on smooth muscle?

A

it binds to receptor on the smooth muscle cell and causes delayed relaxation through an increase in cAMP

61
Q

what receptor mediates NO relaxation?

A

gyanylate cyclase->produces cGMP