Control of Blood Pressure Flashcards
What is the goal of the kidney?
Homeostatic control of blood volume and blood pressure
Changes in blood pressure signal the release of which hormones?
ADH: increases fluid reabsorption
ANP: increases fluid excretion
How do kidneys measure blood pressure?
Kidneys measure GFR as a proxy for systemic blood pressure
How does the glomerular filtration rate (GFR) provide a proxy measure for systemic BP?
Increase in blood pressure -> increase in GFR
Decrease in blood pressure -> decrease in GFR
What is GFR?
Glomerular Filtration Rate: the rate at which blood is filtered through the glomerulus an into the Bowman’s capsule
What is the function of the juxta-glomerular apparatus?
Connects the DCT with the glomerulus
Measures and responds to changes in Na+ concentration in the filtrate
Where are macula densa cells located?
DCT
What are the 3 components of the juxta-glomerular apparatus?
- Macula densa cells
- Juxtaglomerular cells
- Mesangial cells
What do macula densa cells do?
Detect sodium concentration
What do juxtaglomerular cells do?
Adjust the diameter of the afferent arteriole
What are mesangial cells?
Supporting cells
Describe the juxta-glomerular apparatus during homeostasis
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
Describe tubulo-glomerular feedback when there is an increase in BP
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
Describe how tubulo-glomerular feedback regulates systemic BP
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)
Where is angiotensinogen produced?
In the liver
Describe the renin-angiotensin-aldosterone system (RAAS)
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)
What effect does angiotensin II have on BP?
Increase BP through vasoconstriction
What effects does angiotensin II have on blood volume?
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
Where is ANP produced and what effect does it have on RAAS?
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
What are some of the causes of Chronic Kidney Disease (CKD)?
Hypertension, diabetes, kidney infections, glomerulonephritis, polycystic kidney disease, kidney stones, long-term use of NSAIDs
What are the symptoms of chronic kidney disease (CKD)?
Hypertension, nausea, oedema (ankles, feet, lungs), blood/protein in urine, anaemia, weak painful bones
What is furosemide?
A diuretic
Rid the body of extra fluid or salt
What are the consequences of CKD?
Inadequate removal of fluid and waste products of metabolism
Inappropriate activation of RAAS
How is chronic kidney disease treated?
- 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)
