Lecture 19: Fluid Balance
Silverthorn Chapter 20
Introduction
How is urine production fine-tuned? How do your kidneys know when to produce dilute urine and when to produce concentrated
urine? Dilute urine (few particles/volume)? Concentrated urine (many particles/volume)?
Several pieces of info are compiled to help determine what kind of urine to produce…but we focus on ONE…
ECF osmolarity
1. Detected by receptors in the body that detect blood concentration: osmoreceptors (they are found in the vessel walls in the
hypothalamus and they detect STRETCH)
A. If osmotic pressure in the blood increases (blood conc increases), osmoreceptors in the hypothalamus SHRINK
B. Osmoreceptors fire more often when they SHRINK (so they detect INCR osmolarity and respond by firing an action
potential)
C. WHEN the blood is less than 280 mOsm, they stop firing, indicating all is cool.
D. When blood osm goes higher than 280, they begin firing, indicating a blood concentration imbalance
2. How can you increase ECF osmolarity?
A. Decreasing volume
B. Increasing solute concentration
3. How can you decrease ECF osmolarity?
A. Increase volume
B. Decrease solute concentration
Note: Blood pressure and kidney function are intimately intertwined…
Two major hormones are involved in fluid homeostasis:
1. Aldosterone- adrenal cortex
2. Antidiuretic hormone (ADH…aka vasopressin)- anterior pituitary
Blood pressure and the KIDNEYS
1. Low sodium is detected by macula densa cells in the end of the ALH (beginning of DCT)…this indicates low BP
A. Macula densa: Specialized cells in the ALH/DCT that monitor filtrate composition
i. (Note the actual orientation of the nephron…the ALH/DCT actually makes CONTACT with the afferent/efferent
arterioles! This specialized location is the juxtaglomerular aparatus.
2.
3.
4.
5.
6.
a. Juxtaglomerular cells (aka granular ccells) line the afferent/efferent arterioles
b. Macula densa cells line the ALH/DCT
ii. The purpose of this? To allow MONITORING of filtrate composition and to stimulate APPROPRIATE
MODIFICATION based on concentration of filtrate
B. Possible mechanism:
i. Lower BP leads to lower GFR (glomerular filtration rate)
ii. Filtrate stays in nephron longer…
iii. More sodium is absorbed from the filtrate
iv. Macula densa detects lower Na in filtrate
Macula densa cells send a chemical message to afferent arteriole
Afferent arteriole releases renin (an enzyme) into the blood
Renin converts angiotensinogen in the blood to angiotensin I
Angiotensin I encounters “Angiotensin converting enzyme” (ACE), often in the lungs, and is turned into Angiotensin II
Angiotensin II has many powerful effects that INCREASE BP, including:
A. Vasoconstriction (increases BP)
B. Increased cardiac output
C. Increased aldosterone production (in adrenal glands)
i. Increased thirst (due to increased sodium reabsorption)
a. Thirst is stimulated by osmoreceptors in the hypothalamus when plasma osomolarity gets HIGHER than 280mOsm
b. Receptors in the oropharynx detect cold water and stop the firing of thirst receptors, regardless of osmolarity.
D. Increased vasopressin secretion
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Aldosterone
1. Produced in adrenal cortex
2. Acts on the last third of DCT and on the CD that is in the cortex
A. REMEMBER: The cells here are impermeable to water!
3. Increases reabsorption of Na+ into blood
4. Aldosterone secretion is stimulated by:
A. Decreased blood pressure (via the Renin-angiotensin-aldosterone system of maintaining BP…see above)
B. Too much K+ (hyperkalemia) stimulates a reflex that increases aldosterone production and K+ excretion
5. Mechanism of action (Fig 20-12)
A. Causes reabsorption of Na+ from DCT and CD…also causes increased secretion of K+
B. Acts primarily on principal cells in the CD and DCT (vs intercalated cells, which play a role in acid base homeostasis)
i. Increases luminal permeability to Na and K by keeping existing channels OPEN
ii. Inserts NEW Na and K channels into the luminal membrane
iii. Increases activity of Na/K pumps in basolateral membrane
iv. Result: DILUTE URINE IF ACTING ALL BY ITSELF…
Vasopressin (ADH)
See PAGE 657 IN YOUR TEXT FOR MORE DETAILS.
1. Enables increased reabsorption of water from DCT and collecting duct
2. Reabsorption depends only on the concentration of the interstitial fluid surrounding the collecting duct
3. Stimulation of production:
A. Many receptors in the body that detect blood concentration: osmoreceptors (they are found in the vessel walls and they
detect STRETCH)
i. If osmotic pressure in the blood increases (blood conc increases), osmoreceptors in the hypothalamus SHRINK
ii. Osmoreceptors fire more often when they SHRINK (so they detect INCR osmolarity and respond by firing an action
potential)
iii. WHEN the blood is less than 280 mOsm, they stop firing, indicating all is cool.
iv. When blood osm goes higher than 280, they begin firing, stimulating vasopressin production in the posterior pituitary,
and water reabsorption (also stimulates THIRST!!!).
B. Blood pressure receptors and blood volume receptors can also trigger the production of ADH
4. Mechanism of action: Vasopressin acts on DCT and CD (Fig 20-6)
A. Water pores are inserted into the walls of DCT and CD cells
i. Water pores are contained on little vesicles…inside the cell
ii. Vasopressin binds to receptors on the cell, stimulating exocytosis of the vesicle and consequent insertion of the water
pore on LUMINAL membrane!
B. Water is reabsorbed, filtrate becomes more concentrated
C. Note: Urine can get as concentrated as 1200 mOsm (as concentrated as the conc grad allows)!
Fast fact: Vasopressin is produces MORE at night… (to increase reabsorption of water, and decrease urine volume!) Kids often do
not have this rhythmic control of the hormone production= bedwetting (nocturnal enuresis). Nasal spray DESMOPRESSIN can help
when taken at bedtime!
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External Brain 19: Fluid Balance
STUDY GUIDE
1. Describe the impact of Vasopressin (aka Antidiuretic hormone, or ADH) on urine concentration. Be able to clearly explain the
hormone’s mechanism of action.
2. Be able to apply your understanding of Vasopressin to various drugs, such as Desmopressin (the nasal spray that helps reduce
bedwetting). This could be an APPLICATION question, where you are given an unfamiliar scenario, and asked to explain it,
based on your understanding of how Vasopressin works.
3. How does Aldosterone work? Where is it produced? What is its general mechanism of action? What stimulates its action?
4. What is the juxtaglomerular aparatus? What is its purpose? Where is it located? Relate your answer to Aldosterone.
5. Relate the following terms: jusxtaglomerular cells, juxtaglomerular apparatus, macula densa
6. Compare and contrast aldosterone and vasopressin.
7. Understand the mechanism by which both aldosterone and vasopressin are produced.
8. How are aldosterone and vasopressin related to blood pressure?
9. How is Angiotensin II produced? When is it produced? What does it do?
Bio 7: Human Physiology
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Spring 2014: Riggs