Renin-Angiotensin-Aldosterone System Flashcards

1
Q

Blood volume regulation

A

Role of RAAS

When BP falls, there is an immediate activation of sensors located in major blood vessels and the heart (baroceptors)

They increase SNS outflow to produce immediate mechanisms to raise BP

Long-term restoration of BP is determined by kidney

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2
Q

How long does BP regulation by kidney take

A

24-48 hours

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3
Q

Functions of the kidney

A

Regulation of pH
Removing metabolic watse products
Production of hormones (e.g. erythropoeitin)
Activation of Vit D

Regulation of osmolarity

  • Regulation of salt concentrations
  • Regulation of extracellular fluid volume
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4
Q

How much of cardiac output does the kidney receive

A

20% of cardiac output

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5
Q

What percentage of blood fluid that enters the glomerulus is filtered

A

20% of plasma

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6
Q

What percentage of plasma filtered into the renal tubule is reclaimed

A

99%

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7
Q

How are afferent arteriole cells specialised

A

Modified SM cells referred to as granular/juxtaglomerular cells

Responsible for hormone Renin secretion

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8
Q

Renin

A

Hormone release the juxtaglomerular/glomerular cells that regulates blood pressure

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9
Q

3 Stimuli for renin release

A

Decreased renal perfusion pressure - less volume traveling to kidney (detected by granular cells)

Decrease NaCl concentration (detected at the macula densa)

Increased sympathetic nerve activity (via activation of beta-1 adrenoceptors by NA)

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10
Q

Mechanism of Renin

A

Angiotensin Converting Enzyme (ACE) converts Angiotensin I into angiotensin II

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11
Q

Where is angiotnensin II made

A

It can be made in various tissues that contain all elements to make angiotensin II locally (e.g. heart, blood vessels, perivascular fat)

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12
Q

Actions of angiotensin II

A

Potent vasoconstrictor - Increases peripheral resistance and hence BP (MAIN EFFECT/PURPOSE)

Enhances sympathetic nerve function

Increases release of aldosterone (adrenal gland)

Promotes Thirst

Release vasopressin (ADH)

Trophic effects in heart and blood vessels (Sustain hypertension, cardiac hypertrophy)

Increase in oxidative stress (endothelial cell damage)

**All its roles somehow serve to increase BP

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13
Q

Actions of vasopressin in CV system

A

Direct vasoconstriction

Increases number of H2O channels in the distal tubules/collecting ducts of the kidney - increases fluid retension

Hence known as Anti-Diuretic Hormone (ADH)

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14
Q

Action of Aldosterone

A

Increase expression of Na+ channels in Kidney tubules

Activates Na+/K+ pump (Retain 3 Na+ ions and lose 2 K+ ions)
Results in retention/rebasorption of Na+ (and water) in body

Draws fluid out of collecting duct to keep it in the body

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15
Q

What does a decrease in blood flow to the kidney lead to

A

Important stimulus for renin release

Occurs with normal variations in fluid intake but also from pathological causes
- Decrease in cardiac output - heart failure
Granular cells not stretched as much; renin release, raise BP, higher afterload so heart has to work harder - Maladaptation

  • Renal stenosis or aortic stenosis (narrowing); so less blood in kidney and renin released - Renin-induced hypertension
  • Hypotensive shock
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16
Q

Hypotensive shock

A

BP is below autoregulatory range for maintenance of cerebral and renal perfusion so consciousness is lost as brain is not getting enough oxygen and vital organ perfusion critically impaired

17
Q

Causes of hypotensive shock

A

Low BP can be due to low cardiac output (CO) and/or peripheral vasodilatation

  1. Haemorrhagic shock - blood loss, low CO
  2. Cardiogenic shock - MI causing loss of myocardial power
  3. Endotoxic shock - bacterial toxins cause marked peripheral vasodilatation
  4. Anaphylactic shock - allergic reaction, histamine release causes vasodilatation and increased capillary permeability allowing fluid to leak and get lost
18
Q

Calculate BP

A

Cardiac Output x TPR

19
Q

Discuss the RAAS during a haemmorage that causes hypotension

A