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What are the three barriers involved in glomerular filtration?
Fenestrated endothelium of glomerular capillaries, basement membrane, and filtration slits of podocytes.
What is the function of the fenestrated endothelium in glomerular capillaries?
Highly permeable; allows most substances through but excludes blood cells (formed elements).
Where do the blood cells excluded by the filtration pores go?
Leave via the efferent arteriole.
What is the basement membrane made of and what does it do?
Proteoglycan gel; viscous, negatively charged, excludes molecules > 8 nm like albumin.
Why are most proteins not filtered through the glomerulus?
Too large or bound to other proteins, which the basement membrane excludes.
What substances are mostly protein-bound and therefore poorly filtered?
Most calcium, iron, and thyroid hormone (TH).
How does protein concentration in blood plasma compare to that in the glomerular filtrate?
Blood plasma = 7% protein; filtrate = 0.03% protein.
How does the protein concentration difference affect COP?
Higher colloid osmotic pressure (COP) in the blood than in the filtrate.
What forms the filtration slits in the visceral layer of Bowman’s capsule?
Podocyte cell extensions (pedicels) wrap capillaries and create 30 nm, negatively charged slits.
What is the role of the filtration slits in the glomerular filtration barrier?
Final barrier that prevents protein and large molecule passage.
What are the four stages of urine formation?
Glomerular filtration, tubular reabsorption, tubular secretion, water conservation.
Where is glomerular filtrate found and what is its composition?
In the capsular space of Bowman’s capsule; like plasma but almost protein-free.
What is tubular fluid and how is it different from glomerular filtrate?
Fluid from PCT to DCT; has had substances added and removed by tubule cells.
Where is urine located and how much does it change after that point?
Fluid from PCT to DCT; has had substances added and removed by tubule cells.
Where is urine located and how much does it change after that point?
In the collecting duct; changes mainly in water content, not solutes.
What is glomerular filtration?
A process where water and some solutes in the blood plasma pass from the capillaries of the glomerulus into the capsular space of the nephron.
What molecules can pass freely through the filtration membrane?
Molecules smaller than 3 nm, such as water, electrolytes, glucose, fatty acids, amino acids, nitrogenous wastes, and vitamins.
Which solutes are unable to pass through the filtration membrane?
Solutes bound to plasma proteins, such as most calcium, iron, and thyroid hormones.
What condition results in the presence of protein in the urine?
Proteinuria (albuminuria), which often involves albumin.
What is hematuria and what causes it?
The presence of blood in urine, which can result from kidney infections, trauma, or strenuous exercise that affects kidney perfusion and causes leakage of proteins or blood.
What happens to the kidneys during strenuous exercise?
Prolonged hypoxia can reduce kidney perfusion, causing the glomerulus to deteriorate and allowing proteins and sometimes blood to leak into the filtrate.
What governs glomerular filtration?
BHP (blood hydrostatic pressure) is much higher in the glomerulus (~60mmHg) compared to other capillaries (10-15mmHg).
Why is the BHP higher in the glomerulus?
The afferent arteriole is much larger than the efferent arteriole, creating a large inlet and small outlet.
What is the hydrostatic pressure in the capsular space?
The hydrostatic pressure is ~18mmHg.
Why is the hydrostatic pressure in the capsular space higher than other places?
This results from the high rate of filtration and continual accumulation of fluid into the capsule.
What is the COP of the blood in the glomerulus?
The COP (colloid osmotic pressure) of the blood is ~32mmHg.
What is the COP of the glomerular filtrate?
The glomerular filtrate is almost protein-free and has no significant COP.
What are the pressures involved in filtration in the glomerulus?
An outward pressure of 60mmHg and inward pressures of 18mmHg and 32mmHg, resulting in a net filtration pressure (NFP) of 10mmHg outward.
How does filtration in blood capillaries typically work?
In most blood capillaries, BHP drops low enough at the venous end that osmosis overrides filtration, leading to fluid reabsorption.
How does filtration in the glomerulus differ from other capillaries?
The BHP remains high in the glomerulus, so the capillaries are engaged solely in filtration.
How does high blood pressure affect the kidneys?
It can rupture glomerular capillaries, leading to nephrosclerosis and diminishing renal blood supply.
What are the long-term effects of hypertension on the kidneys?
Hypertension often leads to renal failure, which worsens the hypertension in a positive feedback loop.
What is the glomerular filtration rate (GFR)?
Amount of filtrate formed per minute by both kidneys combined.
How much filtrate does the kidneys produce per minute for every 1mmHg of NFP in a young adult male?
About 12.5 mL of filtrate per minute.
What does the filtration coefficient (Kf) depend on?
Permeability and surface area of the filtration barrier.
What is the GFR for males?
125 mL/min.
What is the GFR for females?
105 mL/min.
What percentage of filtrate does an average adult reabsorb?
99%.
How much urine does an average adult excrete per day?
1 to 2 liters.
What happens if GFR is too high?
Fluid flows through the renal tubules too rapidly, reducing reabsorption of water and solutes, leading to increased urine output and potential dehydration and electrolyte depletion.
What happens if GFR is too low?
Fluid flows sluggishly through the tubules, causing reabsorption of wastes that should be eliminated, potentially leading to azotemia.
How is GFR adjusted?
By changing glomerular blood pressure (BP), which is controlled through renal autoregulation, sympathetic control, and hormonal control.
What is renal autoregulation?
The ability of nephrons to adjust their own blood flow and GFR without external control, helping maintain stable GFR despite changes in arterial BP.
How does renal autoregulation help maintain stable GFR?
It ensures stable fluid and electrolyte balance, preventing excessive urine output even with fluctuations in BP.
What are the two mechanisms of renal autoregulation?
Myogenic mechanism and tubuloglomerular feedback.
How does the myogenic mechanism stabilize GFR?
When BP rises, the afferent arteriole constricts to maintain blood flow into the glomerulus, preventing changes in GFR.
How does tubuloglomerular feedback work?
It adjusts GFR by using feedback from the macula densa in the juxtaglomerular apparatus, which regulates the afferent arteriole’s constriction in response to NaCl levels.
What happens when NaCl levels are high in the loop of Henle?
The macula densa cells secrete ATP, which is converted to adenosine, causing afferent arteriole constriction and reducing GFR.
What is the role of granular cells in tubuloglomerular feedback?
Granular cells secrete renin when BP drops, starting the renin-angiotensin-aldosterone mechanism to restore BP and blood volume.
What is the role of renin in BP regulation?
Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II, a vasoconstrictor that raises BP.
How does angiotensin II affect the kidneys?
It constricts efferent arterioles, raising glomerular BP and GFR, and enhances NaCl and water reabsorption in the nephron.
What is the effect of sympathetic control on GFR?
Sympathetic stimulation constricts the afferent arterioles during exercise or shock, reducing GFR and urine output to redirect blood to vital organs.
How does the renin-angiotensin-aldosterone mechanism raise BP?
By vasoconstriction, promoting NaCl and water reabsorption, stimulating thirst, and constricting efferent arterioles to raise glomerular BP.
Would ACE inhibitors increase or reduce urine output?
ACE inhibitors would increase urine output because they prevent the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone release, which would lower fluid retention.
What are the four major processes in urine production?
Filtration, reabsorption, secretion, and excretion.
Describe the movement of a urea molecule from the blood to the capsular space.
Urea moves from the blood through the glomerular capillaries, across the filtration membrane, and into the capsular space, passing through the endothelial cells, basement membrane, and podocytes.
What homeostatic mechanisms help maintain normal GFR in a dehydrated person with low BP?
Renal autoregulation, sympathetic control, and the renin-angiotensin-aldosterone mechanism would all work to stabilize GFR by constricting arterioles, raising BP, and promoting fluid retention.
What pressure is involved in glomerular filtration?
High blood hydrostatic pressure.
What is the primary filtrate composed of?
Water, electrolytes, glucose, fatty acids, amino acids, nitrogenous wastes, and vitamins.
How does the concentration of solutes in the glomerular filtrate compare to blood plasma?
The concentration of solutes in the filtrate is about the same as in the blood plasma.
What is net filtration pressure (NFP)?
NFP = Blood Hydrostatic Pressure (BHP) – (Capsular Pressure (CP) + Colloid Osmotic Pressure (COP))
What is the blood hydrostatic pressure (BHP) and why is it higher here?
BHP is about 60 mmHg, generated by the heart, and is much higher in the glomerulus than elsewhere.
What is the hydrostatic pressure in the capsular space?
About 18 mmHg, resulting from high filtration rate and fluid accumulation in the capsule.
What is the colloid osmotic pressure (COP) in the blood?
Approximately 32 mmHg, drawing water inward.
How do the afferent and efferent arterioles differ?
Afferent arteriole is wide, efferent arteriole is narrow, and the narrow efferent arteriole continues to form peritubular capillaries (vasa recta).
What are the two mechanisms of renal autoregulation?
Myogenic and tubuloglomerular feedback.
How does the myogenic mechanism stabilize GFR?
Smooth muscle in afferent arteriole contracts when stretched, reducing pressure inside, and relaxes when blood pressure falls, allowing easier blood flow.
What happens when arterial pressure increases?
It stretches the afferent arteriole, causing smooth muscle constriction, which reduces pressure inside the glomerulus.
How does myogenic regulation protect the kidneys from high blood pressure?
It dampens the GFR with increases in blood pressure, preventing dramatic changes in blood flow to the glomerulus.
What is the function of sympathetic control in renal filtration?
It constricts arterioles, reducing blood hydrostatic pressure and GFR, while redirecting blood to vital organs and conserving water.
How does epinephrine affect renal filtration?
It aids in the constriction of arterioles, which reduces blood hydrostatic pressure and filtration rate.
What happens to GFR under sympathetic control?
GFR can be reduced to as low as 3 ml/min.
What is the role of renin release during sympathetic control?
It helps to conserve water and redirect blood to essential organs.
How does ADH influence filtration?
It increases water reabsorption in the collecting ducts, reduces filtration, and leads to more concentrated urine.
What triggers the release of ADH?
Dehydration, loss of blood volume, and rising blood osmolarity stimulate hypothalamic osmoreceptors and baroreceptors.
What does ADH do in the collecting ducts?
It makes the collecting ducts more permeable to water, allowing water to reenter tissue fluid and blood.
How does ADH affect urine formation?
It reduces filtration, leading to more concentrated urine and less water excretion.
What mechanism regulates filtration in response to a drop in blood pressure?
Renin-angiotensin-aldosterone mechanism
What hormone can inhibit the renin-angiotensin-aldosterone mechanism?
ANP (atrial natriuretic peptide)
Where are baroreceptors that detect a substantial drop in blood pressure located?
Aorta and carotid arteries
What happens when a drop in BP is detected by baroreceptors?
Signal sent to brainstem → autonomic reflexes → renin released from kidneys → angiotensinogen from liver converted to angiotensin I
Where is angiotensin I converted to angiotensin II?
Lung and kidney capillaries
What enzyme converts angiotensin I to angiotensin II?
Angiotensin-converting enzyme (ACE)
Where does angiotensin II become angiotensin III?
RBCs and vascular beds
What does angiotensin III trigger?
Aldosterone secretion from adrenal cortex
What are the effects of angiotensin II on blood vessels?
Potent vasoconstrictor; raises mean arterial BP
How does angiotensin II affect the kidneys?
Constricts efferent arteriole → raises glomerular BP and GFR → maintains filtration even when BP is low
What is the effect of efferent arteriole constriction on peritubular capillaries?
Lowers BP → enhances reabsorption of NaCl and H2O from nephron
What effect does angiotensin II have on the adrenal cortex?
Stimulates release of aldosterone
What is the function of aldosterone?
Promotes Na+ and H2O reabsorption in DCT and CD
Where does angiotensin II directly stimulate reabsorption?
PCT (proximal convoluted tubule)
What hormone does angiotensin II stimulate from the posterior pituitary?
ADH (antidiuretic hormone)
What does ADH do in the nephron?
Promotes water reabsorption by CD (collecting duct)
What behavioral response does angiotensin II stimulate?
Thirst and water intake
What class of drugs inhibits the conversion of angiotensin I to II?
ACE inhibitors
What is the overall effect of the renin-angiotensin-aldosterone mechanism?
Raises BP by reducing water loss, encouraging water intake, and constricting blood vessels
What is the major site of reabsorption in the nephron?
PCT
What is the longest and most coiled region of the nephron?
PCT
What percentage of glomerular filtrate is reabsorbed by the PCT, and what else does it do?
~65%, removes substances from blood and secretes them into the tubule
What feature does the surface of the PCT cells have, and why is it important?
Microvilli, increases surface area