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Transcript
Human Anatomy and Physiology
Urinary Physiology—Refer to Text Chapter 26 and other chapters as needed
The following are review questions that can be used to review the basic concepts of urinary
physiology. Please do not limit your knowledge to these questions—use your text and your
laboratory studies as well as the interactive physiology in BA209 (this is required). Here are my
“lecture notes.” I hope this helps those of you who are still struggling to understand this system.
I.
Glomerular Filtration
1. Filtration of the blood occurs through the glomerulus w/in Bowman’s capsule.
Remember, the structure of this filtration membrane is specifically structured for
filtration (see page 1005).
What makes the glomerulus (glomerular capillaries) specially structured for
filtration? (1) large surface area (2) filtration membrane = thin & porous/leaky
w/fenestrations (3)high glomerular capillary blood hydrostatic pressure
2. Describe the principles behind glomerular filtration. Blood in the glomerulus is
under pressure (blood hydrostatic pressure) which forces blood through the
capillary membrane (filtration pressure).
3. Compare the relative diameters of the afferent and efferent arterioles and explain
the significance in this size differential. The afferent arteriole is wider than the
efferent arteriole which means that blood enters the glomerulus through a wider
opening than the blood exiting the glomerulus, thus creating an increased “back
pressure” (=hydrostatic filtration pressure). They hydrostatic pressure is higher in
the glomerulus than in other capillaries. By varying the size of the afferent and/or
arterioles, the glomerular filtration rate (GFR) may be increased or decreased.
4. What percentage of water and solutes of the blood becomes filtrate (primitive
urine)? 20% of the water in the blood is filtered out to become part of the filtrate.
This produces 180 liters of water (potential urine) a day. All solutes present in the
blood (excluding proteins, especially larger proteins such as albumin) including
ions (such as Na+, Cl-, HCO3-, etc.), glucose, amion acids, creatine, and uric acid
are also filtered out of the blood to become part of the filtrate (primitive urine).
Remember that most of these solutes will be completely or at least partially
reabsorbed later on in through the renal tubules. Most of the water will be
reabsorbed too—all but about 1-2 liters, which will be excreted as urine. (Study
normal and abnormal constituents of urine-Table 26.6).
5. What is NOT filtered out through glomerular filtration due to their large size?
Proteins, especially larger proteins such as albumin, fibrinogen and globulins.
RBC’s and other large molecules are not filtered out either.
Thinking about proteins: Glomerularnephritis (inflammation of the glomerulus)
increases the permeability of the glomerular filtration membrane. Now proteins
leak through the membrane and are filtered out into the filtrate (primitive urine)
with no way to be returned to the blood later on. This then increases the capsular
osmotic pressure (see Fig. 26.9) as well as the osmotic pressure within the renal
Revised Spring 2006
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Human Anatomy and Physiology
Urinary Physiology—Refer to Text Chapter 26 and other chapters as needed
tubules while decreasing the osmotic pressure within the capillaries and within the
entire vascular system. Why would this condition cause edema in other areas of
the body—refer back to cardiovascular system, “Edema, where did I go wrong?”
6. Where are the juxtaglomerular cells located? The juxtaglomerular cells (modified
smooth muscle fibers) are located within the walls of the afferent arteriole and are
closely situated next to the macula densa cells in the end of the ascending limb of
the loop of Henle just before it enters the DCT. (see Fig. 26.6) The
juxtaglomerlular cells w/ the macula densa make up the justaglomerular apparatus
(JGA).
7. What is the function of the juxtaglomerular cells? (See Renal Autoregulation of
GFR, Table 26.2) The juxtaglomerular apparatus (JGA) helps regulate the arterial
blood flow w/in the kidney which then determines the rate of blood filtration by
the glomerulus (GFR). These mechanisms work to maintain a constant GFR at a
localized level (= renal autoregulation)
A. Juxtaglomerular cells: As blood flow increases through the afferent arteriole
(a.a), the juxtaglomerular cells detect stretching due to increased blood
pressure; they contract in response, which narrows the lumen of the a.a.,
which results in decreased blood flow to the glomerulus (=↓GFR). If there is
less blood flow through the a.a. there is less stretching, the a.a. relaxes and
dilates, allowing more blood flow into the glomerulus (=↑ GFR).
B. Macula densa cells are sensitive to increased levels of Na+, Cl- and H20 in the
renal tubule as a result of ↑GFR (due to high systemic blood pressure). Their
response is to inhibit the release of NO. NO normally causes vasodilation of
arterioles as a localized response. Inhibiting NO therefore causes
vasoconstriction of the a.a., which decreases blood flow through the
glomerulus. This brings the GFR back down to normal (=↓GFR). If blood
pressure drops in the nephron, then more NO will be produced, resulting in
vasodilation of the a.a.; which then increases the GFR back to normal.
Remember, these are localized responses to maintain a steady glomerular
filtration rate (GFR). See Table 26.2 p. 1008 for regulation of GFR.
8. What is the function of renin? (See Hormonal Regulation of GFR, Table 26.2 p.
1008 and review Fig. 18.16, p. 643) Renin is produced by the JGC in response to
lowered arterial blood pressure (perhaps due to hemorrhaging). Renin initiates the
Renin-Angiotensin-Aldosterone Pathway. Eventually, Angiotensin II causes
constriction of the afferent arteriole (and also efferent arteriole) resulting in
decreased blood flow to the glomerulus decreased glomerular filtration rate
(=↓GFR). This means decreased urine output (UO) so you conserve fluid and
increase your blood pressure. Note: This response is a systemic response to
lowered blood pressure. This response may also be stimulated by lowered levels
of Na+ in the blood and therefore, in the filtrate.
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Human Anatomy and Physiology
Urinary Physiology—Refer to Text Chapter 26 and other chapters as needed
9. Specialized cells, principal cells, in the last part of the distal convoluted tubule (=
DCT) and throughout the collecting duct (CD) are sensitive to decreased levels of
Na+ in the filtrate. Decreased Na+ levels in the filtrate stimulate the release of
renin, which then activates the renin-angiotensin-aldosterone pathway. As a
result, Angiotensin II, a powerful vasoconstrictor, constricts the afferent (and to
some extent the efferent) arteriole, resulting in ________________ (increased,
decreased) GFR.
10. What happens to the pressure (glomerular filtration pressure) if the diameter of
the afferent arteriole increases? If the a.a. dilates then more blood flows into the
glomerulus which results in increased GFP (=↑GFR) and potentially more urine
output (UO).
11. A decrease in the level of renin results in ↓ Angiotensin II, ↓vasoconstriction of
a.a. (=↑vasodialtion/diameter of a.a.) and therefore =↑GFR.
12. How are afferent arteriole diameter, blood flow, and pressure in the glomerulus
interrelated? (See Neural Regulation of GFR, Table 26.2. Note that the afferent
arteriole and the efferent arteriole can be regulated independently. What happens
if a sympathetic response causes constriction of the afferent arteriole? Think
about what happens if the efferent arteriole is dilated/or constricted. ↑ diameter of
the a.a. = ↑ blood flow into glomerulus and ↑ glomerular filtration pressure and
↑GFR and ↑UO.
13. What effect does ANP (atrial natriuretic peptide) have on GFR? (See Hormonal
Regulation of GFR Table 26.2 p. 1008) What is the stimulus? When the atria of
the heart are stretched due to increased blood pressure (increased venous return)
the hormone ANP is released. It targets specialized cells in the glomerulus. The
response is to increase capillary surface area which then increases the GFR
resulting in ↑UO and ↓ blood pressure due to decreased blood volume.
We have been focusing on the localized, hormonal, and neural effects on GFR. Some of these
mechanisms are also involved in tubular reabsorption and secretion. We will discuss this in a bit
more detail with Tubular Reabsorption.
II.
Tubular Reabsorption is the movement of substances from the filtrate (urine) in the
renal tubules back into the blood via the peritubular capillaries and the vasa recti. It is
a very discriminating process which involves specialized cells in specific regions of
the nephron (Table 26.1). Only specific substances and certain amounts of those
substances will be reabsorbed in specific regions of the renal tubules.
1. What percent of tubular filtrate is excreted as urine? Only 1%. We make about
150-180 liters of filtrate/day (= about 45 gallons), but only about 1% of the
original filtrate is actually excreted as urine. We produce about 1-2 liters of
urine/day (average = 1 liter), depending on fluid intake and other personal
conditions.
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Human Anatomy and Physiology
Urinary Physiology—Refer to Text Chapter 26 and other chapters as needed
2. What happens to the remaining 99% of the water and dissolved substances in the
filtrate? It is reabsorbed back into the blood.
3. What are the two basic processes of tubular reabsorption? Contrast the two.
(1)
Passive transport
(2)
Active transport
4. List and describe three examples of passive transport. (does not require energy)
(1)
Osmosis (reabsorption of water)
(2)
Diffusion (& facilitated diffusion)
(3)
Electrochemical attraction (where a negatively charged ion (Cl-) is
attracted to and follows a positively charged ion (Na+) and vice versa.
5. Active transport involves __carrier molecules___ to move the transported
molecules through the membrane. Active transport requires the expenditure of
energy (ATP) or the use of antiporters (opposite direction) or symporters (same
direction). Note: each type of transporter has a limited capacity to transport its
product within a given amount of time (= tubular maximum, Tmax, or renal
plasma threshold). When the Tubular Maximum is surpassed, we say the product
“spills over into the urine.” An interesting example is when a person with
uncontrolled diabetes mellitus has hyperglycemia and exceeds his/her Tmax for
glucose (>200mg/ml). The result is glucosuria. Because of the resulting increased
osmotic pressure of the filtrate there will be less reabsorption of water, resulting
in ↑UO and, therefore, dehydration. Remember the “3 polys” associated with
diabetes mellitus (polydypsia, polyuria, polyphagia).
6. Give examples of ions and molecules reabsorbed (via passive and/or active
processes) from the kidney tubules into the renal intersititial spaces and on into
the peritubular capillaries. (Table 26.3) H2O, glucose, amino acids, uric acid,
urea, Na+, K+, Ca2+, Cl-, HCO3-, HPO42-. Note: large proteins such as albumin are
not included in this list. Explain. What happens with glomerular nephritis? What
is the Tmax for proteins?
7. How much water is reabsorbed due to passive and active transport? Osmosis =
85-90% in the PCT, LH, DCT and Active Transport = 5-10% in the latter portion
of the DCT and CD (principle cells) under the influence of ADH.
8. Where does the majority of tubular reabsorption occur? PCT
Note: About 70% of the Na+ is reabsorbed in the PCT. Angiotensin II stimulates
the reabsorption of Na+ and Cl- and water follows by osmosis while aldosterone
stimulates the reabsorption of Na+ and Cl- followed by water in the CD.
9. By the time the filtrate reaches the DCT what major changes have occurred?
(1) +/- 80% of the filtered was has been reabsorbed (PCT). More or less water
will be reabsorbed at the end of the DCT and in the CD depending on ADH level.
(2) glucose has been totally reabsorbed into the blood (PCT)
(3) the majority of the electrolytes, minerals and nutrients have been reabsorbed.
(4) there is an increased concentration of waste products
Revised Spring 2006
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Human Anatomy and Physiology
Urinary Physiology—Refer to Text Chapter 26 and other chapters as needed
10. What are some of the waste products found in the filtrate as it approaches the
DCT? These would normally be found in the urine.
(1) urea
(2) creatinine
(3) uric acid
(4) ammonia
11. Fluid and electrolyte balance of blood and acid base balance of the body is
primarily regulated in the DCT and CD. They are regulated by hormones which
increase/decrease tubular reabsorption and/or tubular secretion. The body has the
ability to secrete a dilute or a concentrated urine, depending on the needs of the
body. Explain how this works. While the pH of the blood is maintained within
very narrow limits of 7.35-7.45 (average =7.4), the urine is much more flexible
with a broader range between 4.6 and 8 (average = 6) depending on the diet and
other conditions/needs of the body. The urinary system helps maintain the proper
pH of the blood by secreting either H+ or HCO3- in the urine—the urine is much
more flexible in its levels and acts as the dumping ground for many excesses.
III.
Regulation by Hormonal Influence
1. What three hormones regulate the amount of fluid and electrolytes conserved or
excreted by the kidneys?
a. Antidiuretic Hormone (ADH)
b. Renin-Angiotensin-Aldosterone Pathway (Aldosterone)
c. Atrial Natriuretic Peptide (ANP)
2. ADH (antidiuretic hormone) is produced by the __hypothalamus__ and is stored
in the __posterior___ ___pituitary gland ___.
3. What is the stimulus for the release of ADH? Osmoreceptors in the hypothalamus
detect decrease in blood volume, increased osmolarity of plasma/extracellular
fluid (=dehydration).
4. What is the target of ADH? Principal cells of the last part of the DCT and
throughout the CD (especially the CD).
5. What effect does ADH have on DCT and CD? Increases the permeability of the
DCT and CD by inserting water channel proteins in the membrane of the principal
cells. This then causes increased reabsorption of water into the blood and
increases hydration (decreases osmolarity of body fluids).
6. Does increased ADH levels cause you to excrete more or less urine? LESS
7. What is the negative feedback mechanism involved in “turning off” ADH
secretion? As the person increases hydration (osmotic concentration of body
fluids (blood) decreases due to increased blood volume), osmoreceptors are no
longer stimulated and the level of ADH decreases.
Revised Spring 2006
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Human Anatomy and Physiology
Urinary Physiology—Refer to Text Chapter 26 and other chapters as needed
Note: ADH is an ANTI diuretic—anti diuresis = decreased urine output. A “diuretic” on the
other hand, would increase urine output. A person with high ABP might take a diuretic such as
Lasix to decrease blood volume via increased urine output. Diuretics work in several ways:
¾ Inhibitors of ADH
U Water = the best diuretic—as water increases ADH decreases
U Alcohol inhibits ADH causing increased urine output and corresponding
headaches and dry mouth (thirst).
U Diabetes insipidus (“watery urine”) = lack of ADH resulting in increased urine
output. See chapter 18 for more detail.
¾ Inhibitors of Na+ reabsorption (if Na+ is not reabsorbed then H2O does not follow by
osmosis)
U Caffeine decreases Na+ and H2O reabsorption resulting in increased urine output,
dehydration and thirst, so drink water to quench your thirst, not coffee or coke.
U Lasix (a common diuretic) for lowering blood pressure
Remember:
Increasing diuresis increases urine output which decreases blood volume.
Decreasing diuresis decreases urine output which increases blood volume.
8. Aldosterone is produced by the _zona glomerulosa in the adrenal cortex ___ of
the __adrenal_______ gland. (See Endocrine LAB)
9. Renin via the renin-angiotensin-aldosterone pathway), in addition to decreasing
the diameter of afferent arterioles, triggers the release of aldosterone.
10. What effects does aldosterone have upon kidney function?
(1) increases Na+ and Cl- reabsorption
(2) increases H2O reabsorption
(3) increases K+ secretion (blood to urine = increases loss of K+)
As a result of increased aldosterone, the body conserves Na+ and H20, increases
hydration, and increases ABP by decreasing urine output.
11. Describe the affect ANP has on fluid and electrolyte balance.
•
Review from Chapter 18: ADH, ANP, Renin-Angiotensin Pathway, Aldosterone—
stimulus, mechanism of action (negative feedback mechanism), and how they influence
fluid and electrolyte balance. These are very important concepts that you must know very
well for exam 5. They will help you pull systems and concepts together.
Revised Spring 2006
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Human Anatomy and Physiology
Urinary Physiology—Refer to Text Chapter 26 and other chapters as needed
IV.
Tubular Secretion
A.
Tubular secretion moves products from the _______blood________ and
___tubule ___ cells into the ______tubular______ fluid (urine).
B.
3 main functions of tubular secretion
1.
Remove wastes such as creatinine, urea, uric acid, etc.
C.
2.
Maintain electrolyte balance (Na+, K+, Cl-, etc.)
3.
Maintain Acid-Base balance of blood (maintain proper pH)
a.
Normal plasma (blood) pH =7.35-7.45
b.
Through tubular secretion the pH of the blood _usually increases_
(becomes less acidic) while the urine becomes more acidic (4.5-8,
average = 6)
c.
This is accomplished by secreting (into urine)
1) H+ (or HCO3- ) as needed
2) ammonia (NH3)/ammonium ion (NH4+)
Mechanisms of tubular secretion
1.
Secretion of Potassium (K+)
a.
Most K+ in the glomerular filtrate is passively reabsorbed by
diffusion in the PCT (urine Æ blood) and also actively reabsorbed
in other areas of the nephron.
b.
Some K+ may be passively secreted by principal cells in the late
DCT and CD through leakage channels in the DCT and CD. This
amount is variable and adjusts for dietary intake.
c.
The Na+/K+ pump mechanism in the DCT and the CD actively
reabsorbs Na+ while actively secreting K+ ions.
d.
Active reabsorption of Na+ out of the tubule into the blood
peritubular capillaries creates a temporary negative charge within
the tubule.
d.
K+ in the peritubular capillary is displaced by Na+ and therefore
K+ is secreted into the urine.
e.
The hormone aldosterone allows for variable secretion of K+ and
simultaneous reabsorption of Na+ by principle cells in the DCT
and CD. Aldosterone increases the activity of the Na+/K+ pumps
and K+ leakage channels and makes new pumps and channels.
Study Renin/Angiotensin/Aldosterone Pathway (chapter 18, page 643).
Note that ↑K+ in blood can stimulate the zona glomerulosa of the adrenal
cortex. ↓aldosterone = ↑K+ (hyperkalemia) which can cause cardiac arrest.
Just as a review: Remember ↑ reabsorption of Na+ and Cl- causes ↑H2O
reabsorption and ↓UO. Remember, the stimulus could have been
dehydration, Na+ deficiency, ↓ABP, hemorrhage or even ↑K+.
Revised Spring 2006
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Human Anatomy and Physiology
Urinary Physiology—Refer to Text Chapter 26 and other chapters as needed
2.
Secretion of Hydrogn ions (H+)
a.
Na+ /H+ antiporters of PCT (reabsorb Na+ and secrete H+) while
also passively reabsorbing HCO3- (an important buffer for the
blood).
b.
Proton pump mechanism of intercalated cells of DCT and CD
secretes H+ against their concentration gradient and urine can
become much more acidic than blood (dumps acid into urine).
Note: the intercalated cells also have a proton pump mechanism
that pumps H+ into the cells and into the blood and antiporters that
move HCO3- into the URINE if the pH of the blood is too high
(alkaline).
c.
How does secretion of H+ work?
1)
Formula:
CO2 + H2O (CA) Æ H2CO3 Æ H+ + HCO3Source for CO2 = cellular respiration
2)
Stimulus:
↑CO2, ↑H, acid internal environment
3)
H+ are secreted into the urine and displace a Na+.
4)
d.
Na+ enters the peritubular capillaries where it joins with
HCO3- to form NaHCO3 (an important buffer for the blood)
So…what’s the point (conclusions):
1) H+ (acid) is removed from blood
2) Na2 conserved and HCO3- reabsorbed
3) NaHCO3 formed which acts as a buffer for other H+ in the
blood. A buffer makes a strong acid weaker.
NOTE: Blood leaving the kidney via the renal vein has a (higher/lower) level
than blood entering the kidney via the renal artery. Blood = ↑pH (less acidic)
3.
Revised Spring 2006
Secretion of Ammonia to raise pH of blood
a.
Back up system Used if acidic for long periods (eg: emphysema/
COPD, retaining CO2)
b.
Normally, the liver converts ammonia to urea (which is filtered out
and is in the urine), which is not as toxic as ammonia. (Note:
Ammonia is a waste product from the deamination of amino acids.
c.
During prolonged increases in H+ concentrations
1)
NH3 (ammonia) is produced by epithelial cells of the DCT
and CD of the renal tubule.
2)
NH3 diffuses readily through the cell membrane into the
urine.
8
Human Anatomy and Physiology
Urinary Physiology—Refer to Text Chapter 26 and other chapters as needed
NH3 accepts a H+ and becomes NH4+, the ammonium ion in
urine.
4)
The cell membrane is impermeable to NH4-, so they are
trapped in the urine.
5)
Na+ is displaced by NH4+, and it goes back into the cells
where it joins with HCO3- to form NaHCO3 which diffuses into the
blood.
3)
d.
So….what’s the point? (conclusions):
1)
You get rid of a H+ = H+ are removed from the body via
urine.
2)
You trap H+ in the urine so they can’t diffuse back into the
blood.
3)
NH3 + H+ Æ NH4+ buffers the URINE (makes a strong acid
=H a weaker acid)
4)
Conserves Na+ and HCO3- Æ NaHCO3 to buffer BLOOD.
Note: HPO42- + H+ Æ H2PO4- is another similar buffering mechanism. The
tubule membrane is also impermeable to H2PO4- so again the H+ is trapped
inside the urine and the urine is buffered.
V.
4.
Due to secretion of H+ and NH4+, the urine is usually acidic with a normal
pH ranging between 4.5-8 (average = 6).
5.
What’s the reason for secreting K+? There is no acid/base balance
connection here. K+ is secreted to rid the body of excess K+ ions and to
maintain the proper fluid and electrolyte balance via aldosterone.
Regulation of Acid-Base Balance—this is very basic, but it works as a review.
1. An increase in H+ ions decreases the pH (or increases the acidity).
2. CO2 joins with H2O to form H2CO3 (carbonic acid) under the influence of
carbonic anhydrase (an enzyme).
3. H2CO3ÆH+ + HCO3- then
4. HCO3- + Na+ ÆNaHCO3 + H+
5. The purpose here is to get rid of excess H+ ions while sending a base (HCO3-)
(i.e., NaHCO3) to the blood.
•
Go to the next handout on Acid/Base Balance, which has been “basically” completed
for you and study it. It should help you pull several systems together. Review what
you know about acid-base balance from the respiratory system and digestive system and
use the Acid Base Balance handout to your best advantage—this means STUDY it well.
Revised Spring 2006
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Human Anatomy and Physiology
Urinary Physiology—Refer to Text Chapter 26 and other chapters as needed
VI.
Micturition (Don’t forget to do this… It won’t be covered in lecture, but will be
on the exam.)
1. Study the anatomy of the bladder
2. After urine formation where does it go? Trace the path through the kidney and on
to the bladder then out of the body.
3. What is micturition?
4. Describe the micturition reflex (in detail).
Revised Spring 2006
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