Control of Blood Pressure Flashcards

1
Q

What is the goal of the kidney?

A

Homeostatic control of blood volume and blood pressure

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2
Q

Changes in blood pressure signal the release of which hormones?

A

ADH: increases fluid reabsorption
ANP: increases fluid excretion

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3
Q

How do kidneys measure blood pressure?

A

Kidneys measure GFR as a proxy for systemic blood pressure

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4
Q

How does the glomerular filtration rate (GFR) provide a proxy measure for systemic BP?

A

Increase in blood pressure -> increase in GFR

Decrease in blood pressure -> decrease in GFR

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5
Q

What is GFR?

A

Glomerular Filtration Rate: the rate at which blood is filtered through the glomerulus an into the Bowman’s capsule

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6
Q

What is the function of the juxta-glomerular apparatus?

A

Connects the DCT with the glomerulus

Measures and responds to changes in Na+ concentration in the filtrate

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7
Q

Where are macula densa cells located?

A

DCT

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8
Q

What are the 3 components of the juxta-glomerular apparatus?

A
  1. Macula densa cells
  2. Juxtaglomerular cells
  3. Mesangial cells
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9
Q

What do macula densa cells do?

A

Detect sodium concentration

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10
Q

What do juxtaglomerular cells do?

A

Adjust the diameter of the afferent arteriole

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11
Q

What are mesangial cells?

A

Supporting cells

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12
Q

Describe the juxta-glomerular apparatus during homeostasis

A

Macula densa cells detect Na+ is within ‘allowed’ limits - sends no signal to juxtaglomerular cells
Afferent arteriole has larger diameter than efferent arteriole
Glomerular pressure is maintained

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13
Q

Describe tubulo-glomerular feedback when there is an increase in BP

A

Glomerular hydrostatic pressure increases -> GFR increases -> Na+ concentration in DCT increases
This is sensed by the macula densa cells
Na+ flows into macula densa cells and water follows. Macula densa cells swell and release adenosine
Adenosine signals juxtaglomerular cells -> constricts afferent arteriole, decreases glomerular hydrostatic pressure
Local effect on kidney -> no effect on systemic BP

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14
Q

Describe how tubulo-glomerular feedback regulates systemic BP

A

Glomerular hydrostatic pressure falls -> GFR decreases -> Na+ concentration in DCT decreases
This is sensed by the macula densa cells
Not enough Na+ flows into macula densa cells -> they shrivel up and release prostaglandins
Prostaglandins tell juxtaglomerular cells to vasodilate afferent arterioles
Renin is released
Activation of the renin-angiotensin-aldosterone system (RAAS)

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15
Q

Where is angiotensinogen produced?

A

In the liver

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16
Q

Describe the renin-angiotensin-aldosterone system (RAAS)

A

Activated in response to fall in BP
Antiotensinogen is released into circulation, cleaved by renin into angiotensin I
Angiotensin I converted into angiotensin II by ACE (angiotensin-converting enzyme)
Angiotensin II rapidly increases BP (it is a potent vasoconstrictor)

17
Q

What effect does angiotensin II have on BP?

A

Increase BP through vasoconstriction

18
Q

What effects does angiotensin II have on blood volume?

A

Restores blood volume by binding target receptors on:
1. Arterioles: vasoconstriction
2. Hypothalamus: thirst
3. Pituitary gland: release of ADH
4. Adrenal cortex: release of aldosterone
Restores blood volume via increased fluid and salt retention

19
Q

Where is ANP produced and what effect does it have on RAAS?

A

Endothelial cells lining the atrial walls of the heart
Baroreceptors located here
Increase in BP detected by endothelial cells -> release ANP
Counteracts the effects of ADH, aldosterone and renin

20
Q

What are some of the causes of Chronic Kidney Disease (CKD)?

A

Hypertension, diabetes, kidney infections, glomerulonephritis, polycystic kidney disease, kidney stones, long-term use of NSAIDs

21
Q

What are the symptoms of chronic kidney disease (CKD)?

A

Hypertension, nausea, oedema (ankles, feet, lungs), blood/protein in urine, anaemia, weak painful bones

22
Q

What is furosemide?

A

A diuretic

Rid the body of extra fluid or salt

23
Q

What are the consequences of CKD?

A

Inadequate removal of fluid and waste products of metabolism

Inappropriate activation of RAAS

24
Q

How is chronic kidney disease treated?

A
  • Diet (reduce salt intake)/weight loss
  • Often a combination of antihypertensive treatments required
  • Diuretics (furosemide)
  • ACE inhibitors/angiotensin receptor blockers (ARBs)
  • Aldosterone agonists (nuclear receptors or sodium channels)
25
Q

What does furosemide target?

A

NKCC2 co-transpoter on the apical membrane of the thick ascending limb
(blocks sodium reabsorption)

26
Q

Describe kidney failure

A

End stage renal disease
Less than 15% kidney function
Dialysis and/or kidney transplant required

27
Q

What are the 2 types of dialysis for kidney failure?

A

Haemodialysis

Peritoneal dialysis

28
Q

What is the purpose of dialysis?

A

Artificial removal of waste, solutes, water and toxins from blood

29
Q

Describe haemodialysis

A

Blood is diverted through machine, processed, cleaned and returned to the body
Patients require 3 treatments a week

30
Q

Describe peritoneal dialysis

A

Dialysis fluid is pumped into the peritoneal cavity and the peritoneum acts as a filter