Vasculature Flashcards

1
Q

functions of endothelial cells

A

physical lining that blood doesn’t adhere to
permeability barrier
regulate transport of macromolecules
mediate angiogenesis
vascular remodelling - detect signals and release paracrine agents that act on adjacent cells
secrete paracrine agents - vasodilators: prostacyclin, nitric oxide (EDRF) and vasoconstrictors: endothelin-1
formation/maintenance of extracellular matrix
growth factors
substances regulating platelet clumping, clotting and anticlotting
synthesise active hormones from inactive precursors
extract/degrade hormones
secrete cytokines in immune response
influence vascular smooth muscle proliferation in atherosclerosis

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2
Q

angiogenesis

A

new capillary growth

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3
Q

vasodilators secreted by endothelial cells

A
prostacyclin
nitric oxide (endothelial derived relaxing factor)
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4
Q

vasoconstrictors secreted by endothelial cells

A

endothelin-1

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5
Q

2 roles of arterioles

A

in individual organs are responsible for determining relative blood flows to organs at any given MAP
major factor in determining MAP

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6
Q

flow

A

function of pressure gradient and resistance to flow

F = deltaP/R

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7
Q

tank analogy

A

pressure reservoir = arteries. Have such large radii that they provide little resistance to flow.
variable resistance outflow tubes = arterioles. smallest arteries offer significant resistance to flow, but narrower arterioles have major resistance. Less flow and pulse pressure.

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8
Q

blood flow through any organ

A

F = MAP/resistance(organ)

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9
Q

how can resistance of arterioles be changed?

A

arteriolar smooth muscle has spontaneous activity - intrinsic tone

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10
Q

spontaneous activity

A

contraction independent of neural, hormonal or paracrine input

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11
Q

intrinsic/basal tone

A

spontaneous contractile activity of arteriolar smooth muscle
sets baseline level of contraction which can be increased or decreased by external signals
increase in contraction force above intrinsic tone causes vasoconstriction, vice versa for vasodilation

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12
Q

mechanisms controlling vasoconstriction and vasodilation

A

local controls

extrinsic/reflex controls

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13
Q

local controls

A

independent of nerves or hormones
organs and tissues alter their own arteriolar resistances, thus blood flow
includes changes by autocrine and paracrine agents

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14
Q

where is self-regulation apparent?

A

active hyperemia
flow autoregulation
reactive hyperemia
local response to injury

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15
Q

active hyperemia

A

most organs manifest an increased blood flow when metabolic activity is increased

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16
Q

hyperemia

A

increased blood flow

17
Q

factors causing arteriolar smooth muscle to relax in active hyperemia

A

local chemical changes in ECF surrounding arterioles from metabolic activity

18
Q

local chemical changes in ECF surrounding arterioles

A

decrease in conc of oxygen, used in oxidative phosphorylation
increase in CO2
increase in H+, e.g. from lactic acid
increase in adenosine
increase in K+ - action potential repolarisation
increase in eicosanoids - breakdown product of membrane phospholipids
increase from osmotically active products from breakdown of high molecular weight substances
increase in bradykinin, peptide generated from kininogen by enzyme kallikrein secreted by active gland cells
increase in nitric oxide, secreted by endothelial cells

19
Q

bradykinin

A

peptide generated from kininogen by enzyme kallikrein secreted by active gland cells

20
Q

where is active hyperemia highly developed?

A

skeletal muscle, cardiac muscle and glands

21
Q

flow autoregulation

A

changes in arteriolar resistance when a tissue or organ experiences a change in blood supply due to a change in pressure
tries to keep flow constant

22
Q

flow autoregulation mechanism

A

same metabolic factors for active hyperemia

myogenic responses - decreased