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PBL SEM 2 > PBL 6 - regulation of vascular tone via calcium signalling > Flashcards

PBL 6 - regulation of vascular tone via calcium signalling Flashcards

1
Q

what do global cytoplasmic calcium levels determine?

A

contractility

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2
Q

what do localise calcium signals within the cytoplasm do?

A

activate nearby K+ channels to cause hyperpolarisation and thus vasodilation

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3
Q

how do we treat patients with small vessel disease of the kidney?

A

dialysis (bypass kidney)

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4
Q

how do we treat patients with small vessel disease of the eye?

A

use laser gun to photocoagualte the retina — burn away all the dysfunctional arteries

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5
Q

how do we treat patients with small vessel disease of the brain (eg. vascular dementia)?

A

no treatment — institutional care

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6
Q

what are 3 macro vascular complications of when small arteries don’t function properly?

A
  • stroke
  • heart disease
  • peripheral vascualr disease
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7
Q

what are 3 micro vascular complications of when small arteries don’t function properly?

A
  • diabetic retinopathy
  • diabetic nephropathy
  • diabetic neuropathy
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8
Q

describe the endothelial lining of blood vessels

A
  • monolayer

- endothelial cells run parallel to flow

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9
Q

describe the vascular smooth muscle of blood vessels

A
  • vascular smooth muscle cells wrap around the lumen of the artery
  • constrict — lumen gets smaller
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10
Q

what separates the endothelial monolayer from the thick muscular wall?

A

internal elastic lamina

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11
Q

equation for mean BP

A

BP = CO x TPR

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12
Q

what determines whether a vascular smooth muscle cell constricts or relaxes?

A

it’s electrical membrane potential (their electrical activity)

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13
Q

what is the most numerous ion channel in the plasma membrane of vascular smooth muscle cells?

A

K+ channels

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14
Q

what happens when K+ channels open?

A
  • K+ leaves the cell as an intracellular ion

- hyperpolarisation — cell becomes more -ve

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15
Q

what happens when K+ channels close?

A
  • inside of cell becomes more +ve = depolarisation
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16
Q

in what layer are smooth muscle cells located?

A

tunica media

17
Q

describe a cross section of a blood vessel wall

A
  • endothelium
  • tunica intima
  • IEM
  • tunica media — smooth muscle
  • EEM
  • tunica externa
18
Q

how do changes in the membrane potential effect of the contractile of the artery?

A

by influencing the activity of voltage-dependent calcium channels

19
Q

what happens when the MP is lowered to result in reduced contractility of the artery?

A
  • the cell becomes hyperpolarised due to K+ efflux
  • voltage-dependent calcium channels become inactivated
  • less Ca++ can enter the cytoplasm globally
  • reduced contractility of the artery

opposite when cell is depolarised

20
Q

what is the link between K+ and vasodilation/vasoconstriction?

A

K+ channels open = K+ leaves cell = vasodilation

K+ channels close = K+ doesn’t leave cell = vasoconstriction

21
Q

what is the main channel that significantly impacts the resting tone of the small artery?

A

large conductance calcium-activated K+ channel = BKca

22
Q

describe large conductance calcium-activated K+ channels (BKca)

A
  • voltage dependent

- activated by small, very high concentrations of Ca++ — calcium release events from the sarcoplasmic reticulum

23
Q

what causes contraction of arteries?

A

pressure — don’t contract and relax, just squeeze

24
Q

how does pressure affects arterial Ca++ and hence lead to constriction?

A

increase in pressure = increase in arterial Ca++

  • increase in intraluminal pressure
  • artery stretches
  • senses Ca++ in cytoplasm
  • contractile process so therefore the artery squeezes
25
Q

what happens if a drug blocks the voltage-gated Ca++ channels?

A
  • no rise in arterial Ca++

- when the artery is stretched, it doesn’t constrict

26
Q

describe the dual role of Ca++

A
  1. the global level of Ca++ determines how hard the artery squeezes
  2. Ca++ is released by the vascular smooth muscle endoplasmic/sarcoplasmic reticulum as small ‘release events’ = calcium sparks — activated the K+ channels to cause hyperpolarisation
27
Q

describe how intraluminal pressure leads to pressure induced constriction

A
  1. intraluminal pressure
  2. membrane depolarisation (K+ channels close)
  3. voltage gated Ca++ channels
  4. rise in global levels in cytoplasm
  5. pressure induced constriction
28
Q

how does a calcium spark lead to relaxation of a artery?

A
  1. calcium spark
  2. activation of calcium sensitive potassium channels (BK)
  3. efflux of K+ from cell
  4. membrane hyperpolarisation
  5. inactivation of voltage dependent calcium channels
  6. reduction in free cytoplasmic calcium
  7. relaxation
29
Q

what is meant by spontaneous transient outward currents (stoc)?

A

the outward movement of K+ due to the calcium sparks through BK channels (calcium-sensitive K+ channels)

each upward deflection is the calcium spark activating about 30 adjacent BK channels, which then open and K+ leaves down its conc grad, measured as an upward deflection

30
Q

what are the 2 different pathways triggered by intraluminal pressure?

A
  • constriction and vasodilatory pathways
31
Q

what happens when BK channels are pharmacologically switched off?

A

the artery constricts

  • no efflux of K+ from cell
  • depolarisation
  • activation of voltage gated Ca++ channels
  • increase in free cytoplasmic calcium
  • constriction
32
Q

what do we say BK channels are like at baseline?

A

switched on

33
Q

what are the 2 opposing forces present in arteries?

A
  • main force = constriction in response to pressure

- vasodilation from Ca spark induced BK channel hyperpolarisation

34
Q

what happens if the vasodilation from Ca spark induced BK channel hyperpolarisation is lost?

A
  • increased constriction of resistance arteries
  • loss of local auto regulation and hypertension
  • MICROVASCULAR DISEASE
35
Q

name some endothelial things regulated by intracellular Ca++ levels

A
  • barrier function
  • release of NO
  • release of prostaglandins
  • release of hyperpolarising/dilating factors (EDHF)
36
Q

describe 3 different vasodilatory pathways

A
  1. release of nitric oxide
  2. release of prostacyclin (COX pathway)
  3. endothelial dependent hyperpolarisation (EDH)

predominately = vasodilatory function

37
Q

what is the role of of endoplasmic (endothelial) and sarcoplasmic (myocyte) reticulum?

A

store of calcium — when they release calcium, it activates adjacent calcium-activated K+ channels to cause an efflux of K+ out of the cell

38
Q

calcium spark vs. calcium pulsar

A
  • CALCIUM SPARK — this is the calcium release event from SR in the vascular smooth muscle cell. sensitive to intraluminal pressure. activates the calcium-activated K+ channel to cause an efflux of K+ — reduces membrane depolarisation
  • CALCIUM PULSAR = Ca++ signals release from ER in endothelial cell — activates calcium-activated K+ channels — hyperpolarises endothelial cell — this hyperpolarisation is directly d=transmitted through to the vascular smooth muscle cell
39
Q

through what channels in the membrane of the SR does Ca++ leave?

A

Ryanodine Receptor (RyR)

PBL SEM 2 (44 decks)

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