Formation of Urine Flashcards
5 major stages of urine formation:
1) Glomerulus: filtration of blood
2) PCT: re-absorption of filtrate; secretion
into tubule
3) Loop of Henle: concentration of urine
4) DCT: Modification of urine
5) Collecting duct: final modification of urine
Glomerular filtration: hydrostatic pressure:
pushes fluid out of blood vessel into glomerulus = afferent (largest)
pushes fluid into blood = efferent (smallest)
Glomerular filtration: Osmotic Pressure:
pushes fluid into the afferent
Net filtration pressure =
hydrostatic - osmotic - hydrostatic
45-25-10 = 10
Net filtration of glomerulus must be
positive
Renal Blood Flow is subject to autoregulation over a wide systemic BP range.
Autoregulation due to:
- Myogenic: due to response of renal
arterioles to stretch (starlings
law). If BP decreases, renal
artery and effernt arterioles
constrict to maintain constant
RBF - Metabolic: renal metabolites modulate
afferent and efferent arteriolar
contraction
The afferent and efferent arterioles
Changes in GFR can also alter systemic BP
- drop in filtration pressure (hypotension)
can cause drop in GFR - reduced GFR - reduced Na= entering PCT
- macula densa senses a change in tubular
Na+ levels - stimulates juxtaglomerular cells to release
renin - renin release; generation of angiotensin II
- angiotensin II is a vasoconstrictor leads to
an increase in BP - increased BP causes filtration pressure to
increase and GFR returns to normal
Re-absorption and Secretion in the Nephron
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Re-absorption from PCT:
- 65% filtered water, NA+, HCO3-, CL-, K+ and
urea are reabsorbed - Complete re-absorption (almost):
- glucose
- amino acids
- small amount of filtered proteins
- Transcellular routes involve aquaporin
channels on apical and basolateral surfaces - no active water re-absorption; only
osmosis
*Driving force for this re-absorption is
Na+/K+ATPase
Na+ Re-absorption from PCT:
- Na+/K+ATPase pumps 3 Na+ from cells into
peri-tubular capillaries against chemical
and electrical gradients - requires ATP
- Cl- follows Na+ by diffusion and
**Phosphate and sulphate co-transported
with Na+ - glucose is co-transported into the PCT with
Na+
Glucose Re-absorption from PCT:
**Glucose in PCT co-transported with sodium into the PCT walls via theSGLT2cotransporter
Smaller amino acids also transported in this way
Once in tubule wall, glucose and amino acids diffuse directly into the blood capillaries along concentration gradient
Na/K sodium ion active transport pumps, remove sodium from tubule wall and into the blood, maintaining a sodium concentration gradient in the proximal tubule lining
Very little K+ is re-absorbed in the PCT.
True or False?
False
70%
mostly passively via tight junctions
Urea re-absorption in the PCT is passive.
True or False?
True
40-50% of urea
Secretions into PCT:
2 types of specilaised pumps:
1) Organic Acid pumps: uric acid, diuretics,
penicillin
2) Organic Base pumps: Creatinine
The PCT Re-absorption and Secretion
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Re-absorption in the Loop of Henle can be divided into two stages:
1) Re-absorption of water in the descending
limb
2) Re-absorption of Na+ and Cl- in the
ascending limb
Re-absorption: Thin descending limb:
- no active transport of salts
- freely permeable to water via Aquaporin 1
channels - water leaves filtrate and enters interstitial
fluid
Re-absorption: Thick ascending limb:
- tubular wall is impermeable to water
- ** specialised Na/K+/2Cl- co-transporters
- Na+, K+, Cl- re-absorbed into interstitial
fluid
Loop of Henle:
where is the fluid in the loop isotonic, hypotonic, hypertonic?
- isotonic: fluid entering LOH from PCT
water re-absorbed out of descending limb
By the tip of ascending, the filtrate is very concentrated
- hypertonic: water finished re-absorbing
Solutes are then pumped out the ascending limb
- hypotonic: filtrate entering DCT
Loop of Henle: Countercurrent multiplication:
- creates a large osmotic gradient within the
medulla - facilitated by Na+/K+/2Cl- co-transporter in
ascending limb of LOH - permits passive re-asborption of water
from filtrate in descending loop of Henle
Countercurrent Multiplication: Effect of urea on osmolality:
- urea freely filtered at glomerulus
- some re-absorption in PCT
- LOH and DCT relatively impermeable to
urea - urea absorbed from the inner medullary
collecting duct - urea secreted into the thick ascending limb
- urea can diffuse out collecting duct into
medulla down conc grad
Loop of Henle
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The distal convoluted tubule re-absorption and secretion:
- active re-absorption and secretion
- Na+ and Cl- actively re-absorbed in
exchange for K+ or H+ secreted into
tubular fluid
DCT: Re-absorption: NA+/K+
- Na+ exchanged for K+ in late DCT/early
collecting duct - involves PRINCIPAL CELLS
- sensitive to ALDOSTERONE
DCT: Re-absorption: Na+/H+:
- Na+ exchanged for H+ in DCT and early
collecting duct - involves specialised ALPHA INTERCALATED
CELLS
Renal Actions of Aldosterone:
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so more water and sodium re-absorption hence increases BP, more K+ secreted/excreted
Principal beta intercalated cells
alpha = taller columnar epithelium
beta = shorter, flatter
beta contain chloride bicarb exchanger
The DCT and collecting duct are involved in acid-base regulation:
- alpha intercalated cells: secretes acid via
H+/Na+, reabsorbs
bicarb which is
main buffer - beta intercalated cells: secretes bicarb via
pendrin, reabsorbs
acid
Carbonic anhydrase found in kidney tubules reaction
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ADH in the collecting duct:
ADH in plasma binds to V2 receptors on principal cells in DCT and collecting duct, opening more aquaporin-2 on tubular slide; G-alpha-s
- stops water excretion; increases water re-
absorption - more ADH = more conc urine = less volume
Where is ADH released from?
- posterior pituitary gland
- following hypothalamic input
Maximal Circulating ADH when
- severe dehydration
- collecting duct becomes permeable to
water due to maximal aquaporin 2
insertion - re-absorbs 66% of water in CD, low urine
volume
No circulating ADH
- re-absorption of water occurs at various
sites in the nephron - however no ADH means no/less aquaporin
2 so a large volume of urine
Lack of ADH results in
diabetes insipidus
treated using synthetic ADH
Renin-Angiotensin-Aldosterone-System
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RAAS effects
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