Renin-Angiotensin System Flashcards

1
Q

What happens when blood pressure falls?

A

Immediate activation of sensors located in major blood vessels and heart (baroreceptors)

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2
Q

What do baroreceptors do when there is a fall in bp?

A

Increase sympathetic outflow from the CNS to produce mechanisms to raise bp

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3
Q

What is LT restor2tion of bp determined by?

A

Kidney - organ responsible for regulating volume

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4
Q

Functions of the kidney

A

Regulation of pH (H+ and HCO3-)
Removing metabolic waste products
Production of hormones (e.g. erythropoeitin)
Activation of vitamin D
Regulation of osmolarity (control of solute concentrations)
Regulation of salt concentrations
Regulation of extracellular fluid volume

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5
Q

How much of cardiac output does the kidney receive?

A

20% at rest (a lot compared to its size)

Auto regulation - blood flow stays relatively constant over wide range of arterial pressures

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6
Q

What is reabsorption of fluid in the renal tubule controlled by

A

Hormonal control

Linked with sodium reabsorption

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7
Q

What does the juxtaglomerular apparatus do?

A

Regulates salt and fluid balance

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8
Q

Special cells in the juxtaglomerular apparatus and functions

A

Granular cells and macula densa - sensitive to alteration in salt concentration
Afferent arteriolar - granular cells are sampling the fluid, volume, blood flow, renal perfusion pressure

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9
Q

What releases the hormone renin?

A

Juxtaglomerular apparatus cells

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10
Q

When is renin released?

A

When volume is low

1) decreased renal perfusion pressure
2) decreased NaCl concentration
3) increased SNS activity, activation of beta 1 adrenoceptors

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11
Q

What happens when renin is released?

A

Angiotensinogen produced by liver is broken down by renin into angiotensin I - low reactivity
ACE converts into angiotensin II (found in lungs)
Then converted to aldosterone - volume lost in urine

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12
Q

What is ACE?

A

Angiotensin Converting Enzyme

Found primarily in vascular endothelium in lungs

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13
Q

Can angiotensin II be made locally?

A

Some tissues contain elements to generate angiotensin II
eg. Perivascular fat
Not just a circulating hormone system

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14
Q

Actions of angiotensin II

A

Potent vasoconstrictor - increases peripheral resistance and therefore blood pressure
Enhances sympathetic nerve function
Increases release of aldosterone
Promotes thirst
Release vasopressin (ADH)
Trophic effects in heart and blood vessels (? Sustain hypertension, cardiac hypertrophy) smaller lumen
Increase in oxidative stress (? Endothelial cell damage)

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15
Q

Where is aldosterone released from?

A

Adrenal gland

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16
Q

Action of vasopressin in CV system

A

Direct vasoconstriction
Increases number of aquaporin-2 channels in distal tubules/collecting ducts of kidney - increases fluid retention, producing moe concentrated urine

17
Q

Action of aldosterone

A

Increase expression of sodium channels in tubule cells of kidney
Activated sodium potassium pump, leads to retention of sodium and water in the body

18
Q

What is an important stimulus for renin release? And why?

A

Decrease in blood flow to the kidney
Can be an indicator for pathological causes:
Decrease in cardiac output - heart failure
Renal stenosis/aortic stenosis - renin-induced hypertension
Hypotensive shock

19
Q

What is hypotensive shock?

A

Condition where the blood pressure is below the auto regulatory range for maintenance of cerebral and renal perfusion
Such that consciousness is lost and vital organ perfusion critically impaired

20
Q

Causes of hypotension

A

Low CO and peripheral vasodilation

  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
21
Q

BP equation

A

Cardiac output x total peripheral resistance

22
Q

Compensatory mechanisms when blood pressure falls

A

Decreased renal blood flow - renin released - increased angiotensin II - increased salt and water retention - increases cardiac output -> BP RESTORED
Vasopressin increased - vasoconstriction- increased peripheral resistance -> BP RESTORED
Activation of SNS - increased heart rate - stroke volume increased - increased cardiac output -> BP RESTORED
Activation of SNS - vasoconstriction (NA) - increased peripheral resistance -> BP RESTORED