Lecture 15: Regulation Of Peripheral Blood Flow Flashcards

0
Q

How is arteriolar radius controlled?

A

Radius is dependant on contractile state of smooth muscle in arteriolar wall

  • vasoconstriction: increased contraction ➡ decreased radius
  • vasodilation: decreased contraction ➡ increased radius
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1
Q

Smooth muscle contraction. Remind me how it works again?

A

When Ca2+ enters the cell it binds to calmodulin to form the Ca-calmodulin complex. This activates MLCK which causes the phosphorylation of myosin light chain ➡ this makes myosin ATPase active ➡ crossbridge cycling ➡contraction

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2
Q

What is hyperemia?

A

Higher than normal blood flow

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3
Q

Arteriolar radius and distribution of blood flow

A
  • Flow of blood through an organs is regulated by changing arteriolar resistance in that organ.
  • distribution of cardiac output between different organs can be changed according to need
  • arteriolar resistance is regulated both intrinsically and extrinsically
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4
Q

What is the functions of varying arteriole radius?

2

A
  1. Regulating mean arterial pressure (extrinsic)

2. Controlling blood flow to individual capillary beds (intrinsic)

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5
Q

List the intrinsic factors influencing arteriolar radius?

A

1) arteriolar tone
2) active hyperemia
3) reactive hyperemia
4) myogenic response

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6
Q

Regulation of arteriolar resistance
Intrinsic regulation
A) arteriolar tone

A

Arteriolar tone= contraction of arteriolar smooth muscle in the absence of extrinsic input

  • spontaneous, slow depolarisation of smooth muscle cells ➡ calcium influx and contraction
  • makes it possible to locally decrease resistance below resting value
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7
Q

Regulation of arteriolar resistance
Intrinsic regulation
B) active hyperemia
Also what are the mechanisms of active hyperemia?

A

Active hyperemia= increased blood flow in response to increase metabolic activity

  • increased blood flow to contracting muscles, secreting glands, active intestinal epithelium
  • changes assosiated with increased metabolic activity generally cause vasodilation.
    • ⬆carbon dioxide
    • ⬆potassium
    • ⬆ hydrogen ions
    • ⬇ in tissue oxygen concentration

Mechanism of active hyperemia
CBF slide 17

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8
Q

Regulation of arteriolar resistance
Intrinsic regulation
C) reactive hyperemia
Also what are the mechanism of reactive hyperemia

A

Reactive hyperemia= increased blood flow die to previous restriction in blood flow eg blockage
-quickly restores normal chemical balance to deprived tissue
-changes assosiated with blockage of blood flow cause vasodilation ie metabolises increases and oxygen decreases
-Changes associated with release of blockage cause vasoconstriction ie increased blood flow due to lower resistance, metabolises removed, oxygen increases
-blockages can be
-pathological (eg clots)
-physiological (eg blockage of flow during cardiac or skeletal muscle contraction.)
Mechanisms of reactive hyperemia?
CBF slide 20

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9
Q

What is the differences between active vs reactive hyperemia?

A

Slide 22

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20
Q

Arteriolar radius
Intrinsic regulation
Myogenic response. Explain

A

Myogenic response = contraction of arteriolar smooth muscle in response to stretch.
-Stretch sensitive Ca2+ channels open➡ contraction
-maintains a relatively constant flow even in different arterial pressures because of they are sensitive to stretch.
-safeguards blood supply to brain, kidneys, heart
Eg ⬆arteriolar stretch ➡⬆arteriolar SM contraction ➡⬆ resistance ➡⬇flow (negative feedback)

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21
Q

Arteriolar radius
Extrinsic regulation
Neuronal regulation ➡ sympathetic control of arteriolar radius

A

Postganglionic sympathetic neuron ➡ noradrenaline ➡ a adrenergic receptors ➡ vasoconstriction.
There is a baseline (tonic) activity of the sympathetic NS all the time.
Increased sympathetic activity ➡ increased noradrenaline release➡ vasoconstriction.
Decreased sympathetic activity ➡ decreased noradrenaline released➡ vasodilation.

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22
Q

Arteriolar radius
Extrinsic regulation
Hormonal control of radius
What are the 3 main hormones involved in regulation of arteriolar radius?

A

Adrenaline ➡ vasoconstriction or dilation depending on receptor
Antidiuretic hormone
Angiotensin 2
Both function to vasoconstrict

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23
Q

How does adrenalin control arteriolar radius?

A

Released from the renal medulla in response to sympathetic activity.
-action depends on type of adrenergic receptors in different vascular beds
-GI tract, mostly a (alpha) receptors ➡ vasoconstriction
-skeletal muscles, mostly B (beta) receptors ➡ vasodilation
BETA MAKES IT BIGGER!

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24
Q

ADH, Angiotensin 2 and control of arteriolar radius

A
  • Both stimulate vasoconstriction of arterioles
  • both also involved in increasing water reabsorption in the kidney ➡ blood volume
  • affects peripheral resistance and blood volume, therefore regulators of arterial pressure
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25
Q

Interplay between intrinsic and extrinsic regulation.
What is the deciding factor in determining blood flow to an organ:
Can intrinsic regulation override extrinsic regulation?

A

Extrinsic mechanisms maintain stable arterial pressure, coordinate circulatory system as a whole
-intrinsic mechanisms give the individual organ the blood supply it needs
Coronary and cerebral arterioles:
-sparse sympathetic innervation and efficient myogenic response, intrinsic mechanisms dominate ➡ blood supply matches need.

Working skeletal muscles:
-intrinsic regulation dominates ➡ blood supply matches need
Other organs:
-lack well developed intrinsic mechanisms, at the mercy of extrinsic regulation
-blood supply restricted when cardiovascular system is under stress, to maintain MAP

26
Q

Learn the table on slide 33

A

Do it

27
Q

What are the structures controlling blood flow through capillary beds

A

Capillaries themselves don’t have smooth muscle
-arterioles, metarterioles and precapillary sphincter regulate blood flow through capillary beds.
Pre capillary sphincters: smooth muscle rings, contract and act as valves regulating capillary blood flow
Metarterioles: shut, allows capillary bypass.
Slide 34 for image

28
Q

Precapillary sphincter control flow through capillary beds

A
  • Contribute to slow, intermittent flow through capillaries
  • situation-dependant bypass of capillary beds eg shut down GI capillary beds between meals
  • extrinsic (sympathetic) and dominant local control