regulation of blood flow Flashcards

1
Q

why do organs need to regulate their blood flow (4)

A

to match blood supply to metabolic rate; to allow for efficient delivery of nutrients/removal of waste; increase/decrease heat loss; ensure blood flow to vital organs is maintained in the case of major haemorrhage

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2
Q

how is blood flow controlled (vascular level)

A

change in vascular tone

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3
Q

structure of non-striated vascular smooth muscle

A

single nucleus; membrane has Caveolae (similar to t tubules); dense bodies of a-actin (origin of actin + myosin filaments, similar to sarcomere); unorganised

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4
Q

what extrinsic factors affect vascular tone

A

circulating hormones; autonomic stimulation

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5
Q

what is the ion most important in sm contraction

A

Ca2+; intracellular levels govern contraction; L-type Ca2+ channels are found on vascular smooth muscle -> CCBs can affect contraction

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6
Q

what needs to occur to vsm myosin in order for it to form cross bridges with actin

A

phosphorylation of the light chain

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7
Q

light chain phosphorylation pathway

A

intracellular Ca2+ levels increase -> binds to calmodulin-> Ca2+-calmodulin activates myosin light chain kinase -> MLCK phosphorylates myosin - allows cross bridges to form

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8
Q

what happens to Ca2+ post contraction

A

binds with Calsequestrin in the sarcoplasmic reticulum and is stored there; or is transported out of the cell via Na+/Ca2+ exchanger etc.

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9
Q

an upregulation of what 2 molecules causes VSM to relax?

A

c-AMP (inhibits MLCK) and c-GMP (activates myosin phosphatase)

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10
Q

resistance equation (ohms law)

A

R = flow (V)/pressure (I)

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11
Q

what is autoregulation (blood flow)

A

intrinsic ability of an organ to maintain constant blood flow changes in perfusion pressure in the absence of external neural/hormonal stimuli i.e. constant flow is maintained despite changes in the perfusion pressure

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12
Q

what is the myogenic theory of autoreg

A

stretch receptors in the bv walls are activated -> influx of Ca2+ -> sm contraction -> decreased radius -> flow remains the same despite greater transient blood flow; bayliss myogenic response

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13
Q

what is the metabolic theory of autoreg

A

decrease in blood flow leads to an increase in waste product accumulation -> waste products activate receptors which cause vasodilation (Ca2+ influx etc.) -> blood flow increased back to desired rate

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14
Q

examples of vasodilatory metabolites (9)

A

↓ PO2; ↓pH; ↑ pCO2; ↑ temp; ↑K+; ↑ lactate; ↑osmolality; ↑histamine; ↑ products of ATP breakdown (adenosine, inorganic phosphate)

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15
Q

what is the effect of vasodilatory (waste) metabolites on the lungs

A

vasoconstriction

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16
Q

how does adenosine cause muscle relaxation

A

binds to AT2 receptors -> activates c-AMP -> inhibits MLCK binding -> vasodilation

17
Q

what does eNOS activation lead to

A

brachial artery vasodilation

18
Q

what is endothelin

A

a powerful vasoconstrictor; there are 3 isoforms coded for by different genes; produced as pro-hormone big endothelians, converted by endothelian converting enzyme

19
Q

what are prostoglandins synthesised by?

A

vascular endothelium from arachidonic acid

20
Q

what types of prostoglandins are vasoconstrictors and which are vasodilators

A

VC - F series, serotonin;
VD - E, I series, PGE2/4

21
Q

what can be given to raynauds patients to ease symptoms

A

prostacyclin (PGI2) - vasodiliator

22
Q

what hormones are vasodilators (3)

A

kinins (bradykinin, lysylbradykinin); adrenomedullin; atrial natiuretic peptide (ANP)

23
Q

kinin precursors

A

kininogens

24
Q

how do kinins work

A

act on B2 receptors on endothelial cells, causing a release of NO in endothelial cells

25
Q

role of kinins in clotting

A

plasma kallikrenin acts on HMW kininogen to make bradykinin

26
Q

action of adrenomedullin

A

a depressor polypeptide that inhibits alodsterone; releases NO and increases c-AMP in cells; exerts action through calcitonin receptor like recptor and RAMP2/3

27
Q

action of ANP & BNP (3)

A

secreted from the heart (ANP from atria and BNP from ventricles); lowers BP by antagonising various vasocontrictors - released when the heart is stretched; inhibits renin secretion;

28
Q

circulating vasoconstrictors (4)

A

angiotensin/renin; noradrenaline; urotensin II; vasopressin

29
Q

pre ganglionic NT (ANS)

A

Ach

30
Q

post ganglionic sympathetic NT

A

NA

31
Q

post ganglionic parasympathetic NT

A

Ach

32
Q

what does NA exist alongside in NT vesicles

A

ATP; neuropeptide Y

33
Q

what is the neural mechanism of blood flow regulation

A

regulation of BF that depends on cardiovascular centres in the medulla oblongata

34
Q

what does baroreceptor firing cause (neural mech of BF)

A

reflex via the medullary cardiovascular centre - decreased symp to heart, arterioles, veins; increase parasymp to heart

35
Q

RAAS pathway

A

renin –> angiotensin – (liver)–> angiotensin I – (ACE) –> angiotensin II –> vasoconstriction (↓GFR, ↓urine output); adrenal gland stimulaton –> aldosterone –> ↑Na+ retention, ↑ water retention –> ↑ BP