Regulating Arteriolar Resistance Flashcards Preview

B3. Cardiovascular system > Regulating Arteriolar Resistance > Flashcards

Flashcards in Regulating Arteriolar Resistance Deck (25)
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1
Q

What is Darcy’s Law?

A

Flow = pressure difference / Resistance

2
Q

What factors influence resistance and how do they effect flow?

A

Viscosity & Vessel length increase resistance, therfore decrease flow
Vessel radius exponentially decreases resistance so increases flow

3
Q

Which resistance influencing factor does the body use to regulate flow?

A

The vessel radius because its easily altered

4
Q

If we apply darcy’s law to systemic circulation what do we get?

A

CO = MAP/TPR or MAP = CO x TPR

5
Q

The radius of arterioles is altered to direct blood to certain capillaries beds when needed, why should one constrict for every one that relaxes?

A

Because opening lots of channels will increase vascular volume thus decreasing MAP which will cause overall blood flow to drop and some tissues will become hypoxic

6
Q

Whats the differnce between intrinsic and extrinsic mechanisms?

A

Intrinsic are to do with meeting the selfish needs of a single tissue
Extrinsic mechanisms ensure the whole body TPR and thus MAP remains normal

7
Q

What are the types of extrinsic mechanisms?

A

Neural & Hormonal

8
Q

How do neural extrinsic mechanisms work?

A

Sympathetic Fibres release norepinephrine

  • > Binds to alpha1-receptors in arterioles
  • > Arterioles constrict
  • > Flow through tissues decrease and TPR rises
9
Q

How do hormonal extrinsic mechanisms work?

A

The adrenal medulla releases epinephrine

  • > Binds to alpha1-receptors-
  • > arterioles constrict
  • > Flow decreases and TPR rises
10
Q

What TPR reducing effect does epinephrine have?

A

In some tissues like skeletal & cardiac muscle epinephrine activates beta2-receptors causing arteriolar dilation which reduces TPR

This is part of the redirecting of blood to important tissues during fight or flight

11
Q

What other hormones are involved in long term control of MAP

A

Angiotensin II
Vasopressin (ADH)
Atrial & brain Natriuretic Peptide (prodiuretic)

Mainly involved in renal fluid absorption/excretion

12
Q

What are the types of intrinsic (local) mechanisms?

A

Active (metabolic) hyperaemia
Pressure (flow) autoregulation
Reactive Hyperaemia
Injury Response

13
Q

How does active or metabolic hyperaemia work?

A

Increased metabolic activity of a tissue means a higher conc. of metabolites passes into its blood supply.
In response the endothelium produces EDFR (endothelium derived relaxing factor)
EDFR causes arteriolar dilation so that flow increases and the metabolites are washed out

14
Q

What type of homeostatic mechanism is metabolic hyperaemia/

A

A negative feedback mechanism

15
Q

What is pressure or flow autoregulation?

A

When MAP suddenly decreases flow will decrease and metabolites accumulate in vessels.
Again EDFR is produced -> Arteriolar dilation -> normal flow restored

The same response as metabolic hyperaemia but designed to maintain blood flow when MAP changes instead of altering blood flow to match metabolic activity

16
Q

What is the method of reactive hyperaemia?

A

Extreme pressure autoregulation
An occlusion of the vessels in a tissue means theres no pressure driving the flow. Therefore theres a massive metabolite build up -> Loads of EDFR -> Extreme dilation to try and shift the occlusion.
When the occlusion is removed (by whatever method) the vessels are very dilated so theres a huge abnormal flow through that tissue.

17
Q

What is an injury response?

A

C fibres release substance P
Acts on mast cells stimulating Histamine release
triggers arteriolar dilation which increases flow and vessel permeability to that area.
Essentially the start of an inflammatory response.

18
Q

Some areas of circulation regulate arteriolar differently, which areas are these?

A

Coronary Circ.
Cerebral Circ.
Pulmonary Circ.
Renal Circ.

19
Q

The coronary circulation is differnet in that it recieves most of its blood supply during dyastole rather than systole, Why?

A

During heart contraction (systole) the heart muscle squashes the coronary arteries
Also during systole the aortic valve occludes the aortic sinuses so blood cant pass into the coronary arteries

20
Q

How does the coronary circulation cope with increased demand of exercise?

A

It shows excellant active hyperaemia
It also expresses a lot of B2 receptors so when epinephrine is released the arterioles dilate

These 2 mechanisms swamp any sympathetic arteriolar constriction caused by alpha-1 receptors, specifically in the heart.

21
Q

Why is the cerebral circulation different and how does it do it?

A

It has to remain stable no matter so it shows amazing presssure autoregulation in order to stay constant no matter what happens to the rest of the body.

22
Q

the main function of the renal circ. is filtration, what does filtratin rate depend on?

A

Pressure so is heavily effected by MAP

23
Q

How does the renal circ prevent you excreting all your water every time your BP increases?

A

It shows excellant pressure autoregulation so the renal circ. pressure can be a bit independant of the MAP.

24
Q

Summarize the extrinsic effect?

A

Mainly neural/hormonal
Controls arteriolar radius in order to regulate whole body TPR
Exists to maintain an adequate MAP

25
Q

Summarise the intrinsic effects?

A

Concerned with matching local blood flow to the needs of a tissue.
Metabolic hyperaemia, pressure autoregulation, reactive hyperaemia, injury response.