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Urinary system physiology
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Mechanisms of Urine Formation
The kidneys filter the body’s entire plasma volume 60 times each day
The filtrate:
Contains all plasma components except protein
Loses water, nutrients, and essential ions to become urine
The urine contains metabolic wastes and unneeded substances
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Glumerular Filtration
The fluid that is forced out of capillaries into the Bowman’s space is called glumerular filtrate
Similar to blood plasma without the proteins
Tubular reabsorption and secretion
The fluid in the DCT and PCT is called tubular fluid
Differs from the filtrate because substances are moving in and out the tubules
Water conservation
Occur in the collecting duct
The fluid is called urine
Basic processes of urine formation
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Reminder - Capillary Beds of the Nephron
Every nephron has two capillary beds
Glomerulus
Peritubular capillaries
Each glomerulus is:
Fed by an afferent arteriole
Drained by an efferent arteriole
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Most molecules smaller than 3 nm can pass freely. That includes water, electrolytes, glucose, fatty acids, amino acids, nitrogenous wastes and vitamins
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Glomerular Filtration Filtration is a passive process in which hydrostatic pressure
forces fluid and solutes through a membrane
The glomerulus is more efficient than other capillary beds because:
Large surface area of the filtration membrane
filtration membrane is more permeable
Glomerular blood pressure is higher because
Arterioles are high-resistance vessels
Afferent arterioles have larger diameters than efferent arterioles
Higher BP results in higher net filtration pressure
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Specials characteristics of glumerular filtration Filtration depends on the balance between hydrostatic pressure
and colloid osmotic pressure on both sides of the capillary wall
Blood hydrostatic pressure (BHP) is much higher in the glomerulus (60 mmHg as compared to 10-15)
Hydrostatic pressure in the capsular space is about 18 mm Hg (compared to about 0 in the interstitial fluid).
This is a result of continuous filtration and the presence of fluid in the space.
The colloid osmotic pressure (COP) of the blood is about the same as elsewhere – 32 mm Hg
The glomerular filtrate is almost protein-free and has no significant COP
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Glomerular filtration
Total forces in the renal corpuscle:
Forces that work to move fluid from capillaries into capsular space:
Glomerular capillaries hydrostatic pressure (GHP) – 55-60 mm Hg
Forces that work to move fluid out of capsular space to capillaries:
Blood colloid osmotic pressure (BCOP) – 32 mm Hg
Capsular space hydrostatic pressure (CsHP) – 18 mm Hg
60 out – 18 in – 32 in = 10 mmHg net filtration pressure
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Net Filtration PressureFiltration pressure across the filtration membrane is equal to the blood hydrostatic pressure (BHP) minus the colloid osmotic pressure (COP) in the glomerular capillary and minus the capsular pressure (CP).
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Glomerular filtration rate (GFR)
Amount of filtrate produced by the two kidneys each minute (~125 ml)
Factors that control GFR:
Total surface area available for filtration
Filtration membrane permeability
Net filtration pressure (NFP)
GFR is usually measured over 24 hr and it is about 180 L/day for males and 150 L/day in females
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Regulation of Glomerular Filtration
2 types of mechanisms control the GFR
Renal autoregulation (intrinsic system)
Myogenic mechanism
Tubuloglomerular feedback mechanism
Extrinsic mechanisms
Neural controls (extrinsic system)
Hormonal mechanism (the renin-angiotensin system)
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Intrinsic Controls - autoregulation
Renal autoregulation is the ability of the nephron to adjust the blood flow and GFR without external control
Under normal conditions, renal autoregulation maintains a nearly constant glomerular filtration rate
Autoregulation involves two types of control
Flow-dependent tubuloglomerular feedback – senses changes in the juxtaglomerular apparatus
Myogenic – responds to changes in pressure in the renal blood vessels
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Tubuluglomerular feedback mechanism The juxtaglomerular apparatus (JGA) monitors the fluid entering
the DCT and adjusts the GFR
Components of the JGA:
The granular/juxtaglumerular (JG) cells – enlarged smooth muscle cells in the afferent arteriole.
They respond to the cells of the macula densa to dilate or constrict the arterioles
Act as mechanoreceptors that sense blood pressure
Can release renin when BP decrease
The macula densa is a patch of ET at the start of the DCT (in some books it said to be in loop of Henle) directly across from the JG cell
Sense NaCl concentration in the tubular fluid
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Autoregulation control of GFR
If GFR rises, flow of tubular fluid increases and rate of NaCl reabsorption decreases.
The macula densa sense the change and stimulate the contraction of JG cells
This results in constriction of the afferent arteriole thus reducing GFR
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Intrinsic Controls: Myogenic Mechanism
The myogenic mechanism – base on the tendency of smooth muscle to contract when stretches
BP constriction of afferent arterioles
Helps maintain normal GFR
Protects glomeruli from damaging high BP
BP dilation of afferent arterioles
Helps maintain normal GFR
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Extrinsic Controls – neural control
When the sympathetic nervous system is at rest:
Renal blood vessels are maximally dilated
Autoregulation mechanisms is controlling
Under stress:
Norepinephrine is released by the sympathetic nervous system
Epinephrine is released by the adrenal medulla
Afferent arterioles constrict and filtration is inhibited
The sympathetic nervous system also stimulates the renin-angiotensin mechanism
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Renin-Angiotensin Mechanism – hormonal control
A reduction in afferent arteriole pressure triggers the JG cells release renin
Renin acts on angiotensinogen to release angiotensin I
Angiotensin I is converted to angiotensin II
Angiotensin II:
Causes mean arterial pressure to rise
Stimulates the adrenal cortex to release aldosterone
As a result, both systemic and glomerular hydrostatic pressure rise
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Extrinsic Controls: Renin-Angiotensin Mechanism
Triggered when the granular cells of the JGA release renin
angiotensinogen (a plasma globulin)
resin
angiotensin I
angiotensin converting enzyme (ACE)
angiotensin II
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Reabsorption and secretion Conversion of the glomerular filtrate to urine
involves the removal and addition of chemicals by tubular reabsorption and secretion
Accomplished via diffusion, osmosis, and carrier-mediated transport
Cells of the PCT reabsorb 60-70% of the filtrate volume
Reabsorbed materials enter the peritubular fluid and diffuse into the preitubular capillaries
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Nonreabsorbed Substances
Substances are not reabsorbed if they:
Lack carriers
Are not lipid soluble
Are too large to pass through membrane pores
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Nonreabsorbed Substances
A transport maximum (Tm):
Reflects the number of carriers in the renal tubules available
Exists for nearly every substance that is actively reabsorbed
When the carriers are saturated, excess of that substance is excreted
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Regulation of Urine Concentration and Volume
Osmolality
The number of solute particles dissolved in 1L of water
Reflects the solution’s ability to cause osmosis
Body fluids are measured in milliosmols (mOsm)
The kidneys keep the solute load of body fluids constant at about 300 mOsm
This is accomplished by the countercurrent mechanism
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The loop of Henle and countercurrent multiplication
Countercurrent multiplication –exchange occurs between fluids moving in different directions; the effect of the exchange increased as the fluid movement continues
Between the close ascending and descending limbs of loop
Difference in permeability in two arms:
Thin descending is permeable to water and almost not to solutes
Thick ascending relatively impermeable to both but contains active transport mechanism that pump sodium and chloride ions from tubular fluid to peritubular fluid of the medulla
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Countercurrent multiplication Sodium and chloride are pumped out of the thick
ascending limb into the peritubular fluid by co-transport carriers (Na+-K+/2Cl- transporter)
That elevates the osmotic concentration in the peritubular fluid around the thin descending limb
The result is flow of water out of the thin descending limb into the peritubular fluid and increased concentration of solutes in the thin limb
The arrival of highly concentrated solution in the thick limb accelerate the reabsorption of sodium and chloride ions
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 26.13b
Countercurrent Multiplication and Concentration of Urine
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The countercurrent multiplication:
Creates osmotic gradient in medulla
Facilitates reabsorption of water and solutes before the DCT
Permits passive reabsorption of water from tubular fluid in the collecting system
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Osmotic gradient
The kidney has an osmotic gradient from cortex to medulla
The outer layer of the kidney is isotonic with the blood: ~300 milliosmoles/liter
The innermost layer (medulla) is very hypertonic: ~1200 milliosmoles/liter
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Countercurrent Multiplication and Concentration of Urine
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Solutes and water reabsorbed in the medulla need to be returned into circulation.
Blood enters the vasa recta with osmotic concentration of ~300 mOsm/l
Blood descending in the medulla gradually increases in osmotic concentration because of solute reabsorption (plasma proteins limit osmotic flow out of the blood)
Blood flowing toward the cortex gradually decreases in osmotic concentration mainly because of water flowing into capillaries
Function of the vasa recta
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DCT performs final adjustment of urine by active secretion or reabsorption
Tubular cells actively reabsorb Na+ and Cl- .
In the distal part of the DCT reabsorption of sodium ions in exchange to another cation (usually K+)
The ion pumps and Na+ channels are regulated by aldosterone
The DCT is a primary site of calcium ions reabsorption (regulated by PTH and calcitriol)
Reabsorption and secretion at the DCT
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The concentration of the urine is adjusted in the collecting ducts
The kidney uses osmosis in the collecting duct to control the concentration and volume of urine
The collecting ducts pass through tissue with a very high osmotic pressure in the medulla.
As the urine passes into the collecting duct it first passes through a region of isotonic osmotic pressure (300 milliosmoles/liter) and then through a region of hypertonic osmotic pressure (up to 1200 milliosmoles/liter)
If the collecting duct has low water permeability the dilute urine in the kidney tubule passes through with little uptake of water
If the collecting duct has high water permeability much of the water will be reabsorbed from the collecting duct into the interstitial fluid
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ADH and urine volume The permeability of the wall of the collecting duct varies under the
influence of antidiuretic hormone (ADH).
ADH is released by the posterior pituitary in response to increased osmotic pressure (decreased water or increased solutes in blood).
When ADH reaches the kidney, it increases the permeability of the epithelial linings of the distal convoluted tubule and collecting duct to water, and water moves rapidly out of these segments, eventually into the blood, by osmosis (water is reabsorbed).
Consequently, urine volume falls, and urine concentrates soluble wastes and other substances in minimal water. Concentrated urine minimizes loss of body fluids when dehydration is likely.
If the osmotic pressure of the blood decreases, ADH is not released and water stays in the collecting duct, leaves as part of the urine.
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Aldosterone and urine concentration Aldosterone is a steroid secreted by the adrenal cortex
It is secreted when blood sodium falls or if blood potassium rises
It is also secreted if BP drops (indirectly through the release of renin-angiotensin II that promotes aldosterone secretion)
Aldosterone secreted – increased tubular reabsorption of Na+ in exchange for secretion of K+ ions – water follow
Net effect is that the body retains NaCl and water and urine volume reduced
The retention of salt and water help to maintain blood pressure and volume
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Atrial natriuretic peptide (ANP) and urine volume Secreted from the atrial myocardium in response to high
BP
Has 4 actions that result in the excretion of more salt and water in the urine:
Dilate afferent arteriole and constricts efferent – increase GFR (more blood flow and higher GHP)
Antagonized angiotensin-aldosterone mechanism by inhibiting both renin and aldosterone secretion
Inhibits ADH
Inhibits NaCl reabsorption by the collecting ducts
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A Summary of Renal Function
Figure 26.16b