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Acid-Base Balance
By Sidra Ansari November 22, 2016
Lab Partners:
Benjamin Van
Yvonne Lee
Skyler Suchovsky
I. Introduction
Through a variety of interactions and mechanisms, the renal system serves to maintain
fluid balance, osmolarity, acid base balance, excrete waste products, and produce hormones. The
kidneys of the renal system have functional units called nephrons through which urine forms.
Blood is filtered in the glomerulus and the filtered fluid then passes through a structure called the
Bowmans capsule and then into the proximal tubules. The rate at which the blood is filtered and
filtered fluid is made is known as the glomerular filtration rate (GFR). GFR can be estimated by
measuring creatinine clearance, as we will see later in the lab. Basically, creatinine cannot be
reabsorbed into the plasma and that is why it makes a good marker for estimating GFR. Next, the
filtered fluid goes through the ascending and descending limbs of the loop of Henle and to the
distal tubules. Finally, the distal tubules go to the collecting ducts where the newly formed urine
can leave. Between the proximal tubules and the collecting ducts, reabsorption of electrolytes
and water takes place meaning that it goes back into the blood to be sent out to the body. The rest
In the above anatomy, the renal system maintains fluid balance through appropriate
changes in volume and osmolarity of the extracellular fluid (ECF). For example, the renin-
angiotensin-aldosterone system (RAAS) can respond to low sodium and ECF volume and secrete
renin from the kidneys. The renin in turn causes secretion of angiotensin I, which can be cleaved
into angiotensin II. Angiotensin II goes on to increase ECF volume by secreting vasopressin that
allows water to be reabsorbed into the plasma through aquaporins (APQ-2). Angiotensin II can
also increase thirst and cause secretion of aldosterone hormone that serves to increase sodium
reabsorption. All of these responses are made to correct decreased ECF volume and sodium and
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restore balance and thus homestasis. However, other mechanisms can occur to reverse these
responses in the event of ECF expansion or sodium overload. For example, atrial natriuretic
peptide (ANP) can be secreted to decrease sodium reabsorption and thus water reabsorption
because water follows sodium in the body. Therefore, this is one way to decrease ECF expansion
in the body. We will see more examples of how the renal system deals with ECF expansion later
The renal system can also balance pH through intercalated A and B cells. Intercalated A
cells secrete H+ ions and absorb bicarbonate, while intercalated B cells absorb H+ ions and
secrete bicarbonate. Through these cells the body can rebalance acidosis or alkalosis by
absorbing the appropriate ions and secreting the excess into urine. (Sherwood, 2013)
Therefore, the purpose of this lab was to demonstrate how the renal system regulates
homeostasis through fluid balance by measuring ion concentration, osmolarity and acid-base
balance. For urine flow rate, we expected to see a significant increase in the hypotonic subject
due to the hypervolemic load. We also expected an increase in the isotonic subject, also because
of hypervolemic load. We hypothesized that the alkalosis subject would have an increase in pH
because of increased bicarbonate in the urine. In terms of clearance rate, we expect to see an
increase in GFR for the isotonic and hypotonic subject due to the increased volume and flow
rate. It is expected that the sodium concentration should decrease in the hypotonic subject and
therefore we should have seen a decrease in sodium clearance. For the isotonic subject we
predicted an increase in sodium clearance. Finally, for specific gravity, we hypothesized that
there would be increase in the isotonic subjects and a decrease in the hypotonic subject.
(Sherwood, 2013)
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A complete overview of methods can be found in NPB 101L Physiology Lab Manual
second edition (Bautista & Korber, 2009 pgs 67-73). There were four subjects for this
experiment. The largest male of the group served as the control and did not drink anything. The
hypotonic subject was a short, average weight female. The isotonic saline (0.9% NaCl) solution
subject was an average height, athletic male. Finally, the NaHCO3- solution (2.5%) was
consumed by a short, average weight female. A day before lab, all subjects properly hydrated
themselves and avoided alcohol, caffeinated beverages, and drugs. Also, on the day of lab the
subjects did not exercise heavily and they recorded the time the bladder was emptied about 1-2
hours before lab. For Part 1, the proper amount of solution to be consumed was calculated
according to the body weights of the subjects. In part 2, the solutions were measured accordingly
and brought to the lab table to be ready for consumption following the first urine collection.
Then, the subjects collected their first urine samples and measured the amount urine collected
using graduated cylinders. The urine was collected again at 30 min, 60 min, 90 min, and 120
min. For each sample collected, about 150-200 mL of urine was saved in another cup labeled
with the subjects name and appropriate time. These samples were used to measure the pH of the
urine, the specific gravity, and concentration of sodium while waiting to collect the next urine
sample.
To measure the specific gravity, the tip of the refractometer was inserted into the urine
sample to get an instant reading. To measure the pH of the urine, the tip of a portable pH
electrode was put into the urine sample while the cup was being swirled. The tip of the electrode
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was first cleansed with distilled water and dried with a KimWipe. The same was done after
immersing the electrode and before returning it to the tube containing the buffering solution.
Next, the sodium clearance rate was calculated. First a sodium electrode was cleansed with
distilled water and dried with a KimWipe. Then, the tip was placed in the urine sample, again
while it was being swirled, and the result was recorded. To clean the sodium electrode a 100mM
NaCl solution was used and the tip was placed in 100 mM NaCl as well. A standard curve was
used to convert the mV reading to sodium concentration and that value was then used to
To prepare the urine samples for creatinine concentration measurements, the urine
creatinine concentration and the dilution factor were calculated. Using these values, different
dilutions were prepared to be placed into a spectrophotometer. The spectrophotometer tubes were
labeled with tape near the top of the tube with the name of the subject and time of urine
collection. Next 3.0 mL of alkaline picrate was added to each tube and mixed by gently tapping
the sides of the tube. The tubes were allowed to sit for 8 minutes for the appropriate reactions to
take place and care was given that the tubes did not sit too long. After 8 minutes, the tubes were
placed in the spectrophotometer in the order that the alkaline picrate was added. The absorbance
value was recorded and used to calculate the creatinine clearance rate.
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III. Results
For all graphs a urine sample was not collected at Time = 120 minutes for the alkalosis
subject.
As seen in Figure 1, there is an increase in urine flow rate for the hypotonic subject while
there an initial increase followed by a decrease in flow rate for the isotonic subject. For the
Figure 1: Flow rate of urine in various subjects over a two-hour time period; Isotonic
hypotonic subject, the flow rate did not increase until after the bladder was voided after 60
minutes with a flow rate of 2.700 ml/min. After this, the flow rate continued to increase until it
became steady after 120 minutes with a flow rate of 6.6300 ml/min. For the isotonic subject, we
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see an initial small decrease from a flow rate of 1.2329 ml/min to 0.9 ml/min from the first
bladder voiding to the one done after 30 minutes. Next we see a sharp increase to 7.367 ml/min
after 60 minutes followed be a decrease that continued until the end of the experiment. The
control maintains a steady flow rate around 0.5000 ml/min throughout the two-hour time period.
Creatinine Clearance
graph. Figure 2, shows that there is a decrease in creatinine clearance for the isotonic
subject and also a slight decrease for the hypotonic subject. Furthermore, the isotonic
Figure
subject 2: Creatinine clearance rates for various subjects to estimate GFR; Isotonic
has an unusually high creatinine clearance of about 388 ml/min. This value
decreases to 324 ml/min after a 60 minute time period which is the point of the second
bladder voiding. The hypotonic subject also shows an unusual slight decrease from
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187 ml/min to 126 ml/min. Meanwhile, the controls creatining clrance rate did not
constant decrease in sodium concentration over the two-hour time period. As for the
isotonic subject we see values jumping around with an initial increase from 176.335
mEq/L to 211.038 mEq/L after half an hour. Then there is a dramatic decrease T=60
minutes to 22.244 mEq/L, which stays about the same after an additional half hour but
again dramatically increases back to 213.764 mEq/L. The control maintained a fairly
These values were used to calculate sodium clearance rates and plot a graph
showing the trends over two hours. There is a constant decrease in sodium clearance
for the isotonic subject followed by a sharp increase in sodium clearance shown in
Figure 3. When the bladder was first voided the sodium clearance was 1.499 ml/min
and then decreased to 0.278 ml/min after 90 minutes. From there the sodium clearance
rate sped up to 2.359 ml/min. Though there are slight increases and decreases in the
sodium clearance for the hypotonic the subject there is an overall decrease from 0.632
ml/min to 0.059 ml/min. The control did not have any fluctuations in sodium clearance
Specific Gravity
The specific gravity of urine was taken in order to measure the concentration of
solutes. As seen in Figure 5, the isotonic and hypotonic subjects showed specific
gravity values below 1.025 and the values decreased steadily for the first one and half
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hours before increasing at the end of the two-hour period. For the isotonic subject,
specific gravity started at 1.016 before increasing slightly to 1.0207. Afterwards, the
subject, the specific gravity decreased from 1.0237 to 1.000 between 0-90 minutes,
Urine pH
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In terms of pH, the bicarbonate subject showed the most significant change
where the pH dramatically increased after a slight decrease in the beginning. As seen
in Figure 6, the pH decreased from 7.04 to 6.83. Then in the next hour the pH
looks like there is an overall trend of the pH increasing. Therefore, we probably would
have seen a slightly higher pH at T=120. The controls pH remained stable around
6.7-6.8.
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Table 1 shows values for the amount of water or sodium that should have been excreted
versus the amount of water or sodium that was actually excreted by the subject. More results can
be seen the isotonic and hypotonic subjects. Both subjects excreted significantly more water than
what was expected. The isotonic subject was expected to excrete about 148 ml of water but
actually secreted about four times that amount at 446 ml. The hypotonic subject also showed
similar results where she was expected to secrete 106 ml but instead secreted five times that
amount at 502 ml. As for sodium expected, the isotonic subject surprisingly secreted less sodium
at 0.5833g than what was expected at 0.5984. Meanwhile, the hypotonic subject secreted
significantly less sodium at 0.09662g when she was expected to excrete at least 0.2528 g. The
control excreted a little less water and sodium than what was expected but the difference is not
huge.
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IV. Discussion
In this lab we demonstrated how the renal system maintains homeostasis through fluid,
solute, and acid-base balance. This was done by collecting urine samples over a period of two
hours from four subjects who drank different solutions. The control did not drink anything while
the other three subjects drank either isotonic saline, bicarbonate, or hypotonic (excess water)
solutions. Then flow rate, creatinine clearance, sodium concentration, sodium clearance, pH and
specific gravity were measured. By looking at these parameters we were able to demonstrate
how the renal system responds to changes in extracellular fluid (ECF) volume, solute
By responding to changes in volume in the ECF and solute concentration in the plasma
the renal system is able to balance fluids (Sherwood, 2013). In our case we expanded the volume
of the ECF in the isotonic (Jensen et al., 2013) and hypotonic (Sherwood, 2013) subjects due to
the hypervolemic loads. In terms of solute concentration, no change in the ECF solute
concentration will occur because the solution being consumed has equal concentration of solutes
to the body, hence isotonic. However, the ECF will become diluted in the hypotonic subject
because they are drinking pure water (14 mL H2O/kg). (Sherwood, 2013) The changes discussed
above caused a change in flow rate, glomerular filtration rate (GFR), sodium concentration,
Flow rate is the milliliters of urine voided per minute. We hypothesized that urine flow
rate would increase in the isotonic and hypotonic subject since those subjects experienced a
hypervolemic load (Atherton et al., 1970). As seen in Figure 1, the isotonic subject experienced
an increase in flow rate in an hour time period, after which, the flow rate decreased. In another
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study (Nishimuta, 2006), it was found that consuming 500 mL of 0.9% saline barely changed
urine flow rate and stayed stable for the 4 hour time period. Although, another later graph in the
same study yielded similar results to ours seen in Figure 1, where the flow rate increased to a
maximum and then dropped (Nishimuta, 2006). Also, in a different study where normal rats were
injected with intravenous saline 0.9% solution, an increase in urine flow rate was observed in
microliters/min (Atherton et al., 1970). Therefore, there is research to support our hypothesis and
results of urine flow increasing in isotonic subjects even if our results only showed an increase
for a time period of an hour followed by a decrease. Also seen in Figure 1, the flow rate for the
hypotonic subject increased steadily and slightly plateaued by the end of the two hour time
period. For ingestion of normal water, other research (Nishimuta, 2006) showed an increase in
urine flow rate that resembled the results seen in Figure 1. In fact, between 0-120 minutes the
results look very much alike and the flattened peak in the other experiment (Nishimuta, 2006)
looks similar to the plateau we see in Figure 1. Again our results and other research support our
An increase in flow rate due to hypervolemic load and consequent ECF expansion is a
way for the renal system to maintain homeostasis by returning fluid balance back to normal
(Sherwood, 2013) The increased amount of water, whether from the isotonic or hypotonic
solution, has to be removed from the body through the urine thus increasing flow rate. Water is
removed by decreasing secretion of vasopressin and thus decreasing reabsorption of water back
into the plasma in the distal and collecting tubules. Vasopressin is an antidiuretic hormone that is
decrease in ECF. It then recruits AQP-2, aquaporins or water channels, to the cell surface and
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allows for water to be reabsorbed into the plasma. But when there is too much water, such as in
our hypotonic and isotonic cases, no vasopressin is secreted and AQP-2s cant be recruited for
water reabsorption and instead the water is secreted into the urine thus increasing flow rate
(Sherwood, 2013. One study (Murase et al., 1999) found that water loading in rats caused
volume expansion, increased urine, and of course decreased AQP-2. This supports the
physiology behind why we see an increase in urine flow rate (Figure 1) and water secretion
(Table 1).
In addition, we see proof of excess urine water from our results where actual water
secreted was much higher than what should have been expected in both the isotonic and
hypotonic subjects in normal circumstances before ingestion of fluid (Table 1). Therefore, we
were able to prove our earlier hypothesis that flow rate increases in the isotonic subject (at least
for a while) and hypotonic subjects. Furthermore, we saw fluid balance through regulation of
ECF volume by removing excess water to make up for the expansion in the ECF.
Another way the renal system maintains fluid volume by responding to an expansion is
ECF volume is by increasing GFR. Therefore, we hypothesized that in the isotonic and
hypotonic subject we would see an increase in creatinine clearance due to excess water. As stated
earlier in the introduction, we used creatinine clearance to estimate GFR, because it is not
reabsorbed back into the plasma (Sherwood, 2013). As seen in Figure 2, we saw an unusual
decrease in creatinine clearance, and thus GFR, which did not support our hypothesis. In fact, the
isotonic subjects creatinine levels start at an unusual high of 388 mL/min, meaning that these
results were most likely inaccurate. These unusual results could be a result of improper dilution
preparation, such as not mixing the samples enough. Furthermore, we can see from other
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research that GFR should have increased in both the isotonic and hypotonic subjects. After
infusion of saline 0.9% and subsequent ECF expansion in normal rats, an increase in creatinine
patients were infused with hypotonic solution and still exhibited an increase in GFR due to the
GFR is the rate at which filtered plasma is produced at the glomerulus and it can be
influenced by many factors. But the factor that affects our results, or at least the expected results,
is blood pressure (Sherwood, 2013). Again when we ingest a load of water whether from the
isotonic or hypotonic solution, we expand our ECF and thus increase blood pressure.
Baroreceptors, located in the carotid sinus and aortic arch, can sense the stretch in blood
vessels caused by increased blood pressure and can stimulate the sympathetic nervous system
(Kougias et al. 2010). This allows blood vessels to dilate and increase blood flow because of the
wider and larger space. Therefore, the afferent arterioles that lead plasma to the glomerulus can
also dilate making it easier for blood to flow and thus increase GFR. As a result, more water is
filtered out of the expanded ECF and secreted through the urine in order to return blood pressure
levels back to normal (Sherwood, 2013). This increase for water filtration can again be
accounted for in Table 1, where the isotonic and hypotonic subject excreted more water than
expected. So, yet again we see another way the renal system maintains fluid balance by
accounting for ECF expansion by regulating volume. Consequently, while our results do not
support our prediction of increased GFR in the isotonic and hypotonic subjects, other research
So far we saw two ways ECF volume is regulated to achieve fluid balance. However, in
order to achieve full fluid balance the renal system also has to account for ECF solute
concentration (Sherwood, 2013). In order to study this aspect of renal homeostasis we measured
urine sodium concentration, sodium clearance and specific gravity (concentration of solutes in
specific gravity, and sodium clearance in the isotonic subject. Even though, we are not adding or
taking away from the ECF solute concentration in the isotonic subject, the water is still excreted
out as explained in earlier results, so therefore the sodium in the solution should be as well.
increasing slightly at first and then decreasing rapidly before stabilizing and increasing sharply
again. Also from Figure 5, we see that specific gravity increased slightly, then decreased, and
then increased again towards the end. This trend is consistent with the trend seen in urinary
sodium concentration. Another consistency in trends seen in lab was sodium clearance. Sodium
clearance refers to how much plasma is used to filter a certain amount of sodium (Sherwood,
2013). In our isotonic subject the sodium clearance decreased at first and increased rapidly
towards the end (Figure 4) in conjunction with the rapid increase in urinary sodium concentration
seen towards the end in Figure 3. Therefore, more plasma was needed towards the end to filter
out more sodium. Essentially these three results support each other in that one did not happen
without the other. From Table 1, however, we can see a contradictory result where the isotonic
subject actually excreted less sodium (0.5833g) than what was expected (0.5984g). This
particular result means that the subject should not have an increase in urinary sodium
concentration.
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Upon further research, one study (Udokang & Akpogomeh, 2005) found that giving
isotonic saline solution to healthy undergraduate students increased sodium urine concentration
over the course of 3 hours. In addition, the same study saw an increase in specific gravity in their
isotonic subjects. Further investigation led to another research study (Atherton et al. 1970)
where urinary sodium increased after infusion of 0.9% saline though it was much less .
Therefore, the research shows that our isotonic subject should have seen a steady increase in
sodium concentration due to removal of sodium ions found in the 0.9% saline solution. This
supports our earlier hypothesis that there should have been an increase in urinary sodium
concentration following ingestion of isotonic saline due to the sodium ions found in the solution.
Our results do not support our hypothesis until the towards the end where there is a significant
The increased urine sodium concentration that should have been seen in the isotonic
subject could be explained by release of atrial natriuretic peptide (ANP). One study (Kato et al.,
1986) found that plasma ANP increased following volume expansion through infusion of
isotonic saline solution, possibly due to sodium ions. However, the ANP concentration as a result
of isotonic saline solution was much lower compared to the ANP concentration response during
infusion of more concentrated saline (5%) (Kato et al., 1986). As stated earlier, ingestion of
isotonic saline does not change the solute concentration in the plasma. But there is still sodium
present in the fluid that was ingested and just like water had to be excreted to maintain fluid
balance so does sodium. Therefore, when there is increased sodium or even increased ECF
expansion, as we see in isotonic subjects, ANP is released to inhibit sodium reabsorption back
into the plasma. Instead it is excreted in the urine along with water since water and sodium
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follow each other in the body. Surprisingly ANP also increases GFR which could be another
reason why we see the increase in GFR for the isotonic subject as stated earlier. Therefore,
regulation of solutes also regulates ECF volume. Finally, ANP inhibits renin and aldosterone
secretion in RAAS, both of which would normally react to lowered ECF and sodium and thus
For our hypotonic subject we hypothesized that there would be a decrease in urine
sodium concentration, sodium clearance and specific gravity. In Figure 3, there is a steady
decrease in sodium concentration throughout the two hour period. The specific gravity of the
urine matches this trend except for a small increase from 1.000 to 1.009, which is not too
significant (Figure 5). Also, although there are slight fluctuations in sodium clearance for the
hypotonic subject, but there is an overall decrease (Figure 4) that matches the decrease in sodium
concentration (Figure 3). This means that less plasma was filtered of less sodium in the
hypotonic subject. Looking at other research, a study done on male japanese students
(Nishimuta, 2006) found that there was decreased urinary sodium concentration after ingestion
of 500 mL of water. Another study (Udokang & Akpogomeh, 2005), also found a decrease in
urinary sodium concentration after ingestion of water in healthy undergraduate students. Hence
our hypothesis about urine sodium concentration decreasing in hypotonic subjects is supported
The fall in urinary sodium concentration seen in hypotonic subjects can be explained by
the fact that the renal system will attempt to conserve plasma solute concentration following
excess ingestion of water (Sherwood, 2013). The body is able to conserve solutes while excreting
water by again decreasing secretion of vasopressin, which would normally allow for AQP-2
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recruitment to cell surfaces to allow more water in the plasma. Without their recruitment
however, excess water is excreted in the urine (Sherwood, 2013). The decrease in vasopressin
secretion is caused by osmoreceptors located in the hypothalamus that can detect the decrease in
solute concentration in the plasma caused by excess water (Sherwood, 2013). Therefore, here we
see an example of how the renal system regulates solute concentration in the plasma in order to
bring about balance in the bodys fluids. By removing excess water not only is the renal system
decreasing excess ECF but also making sure the solute concentration remains in balance for
normal function.
Finally, another homeostatic regulation of the renal system studied in this lab was pH
control. We hypothesized that the subject ingesting bicarbonate solution exhibit the most change
and experience a rise in pH. Figure 6, shows a significant increase in pH following a slight initial
decrease. Therefore, our results prove that overall there is an increase in urine pH following
ingestion of bicarbonate. Our results and hypothesis can be further supported by outside
research. In one study, a specially made oral alkalizing solution caused urine pH to significantly
increase in volunteers who drank it (Tolouian et al., 2005). Another study that compared its
results to the above studys results also found that administering an alkalizing tablet increased pH
intercalated B cells and increased bicarbonate in the tubules. In the distal and collecting ducts,
acid-base balance is maintained thanks to the actions of type A and B intercalated B cells found
(Sherwood, 2013). Type A intercalated cells are responsible for secreting H+ ions and
reabsorbing bicarbonate ions back into the plasma. On the other hand type B intercalated cells
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secrete bicarbonate and reabsorb H+ ions back into the plasma (Kim et al., 1999). In our case,
type B cells are important and their activity increases during bicarbonate loading in order to
oppose alkalosis. Essentially, they secrete more bicarbonate into the urine and reabsorb H+ ions
to return acid-base balance to normal. Another factor contributing to increased bicarbonate in the
urine is the fact that bicarbonate starts to collect in the tubular fluid and cannot be reabsorbed.
The reason it cannot be reabsorbed is because it has to first combine with H+ ions and then be
broken down again by carbonic anhydrase to start the process of entering the plasma. But if there
is more bicarbonate ions than H+ ions then bicarbonate will be excreted due to the lack of H+
ions. Thus these mechanisms regulated by the renal system allow for the body to recover from
In conclusion, we were able to see how the renal system maintains fluid balance by
regulating ECF volume and osmolarity. In addition, we saw acid-base balance through increased
actions of type B intercalated cells which helps the body come back from alkalosis. An
expansion in ECF volume is corrected by increasing flow rate and glomerular filtration rate to
put more water out in the urine. Also, reabsorption of water back into plasma is decreased
excess solutes or by retaining them in plasma. One way to lose solutes is through the actions of
ANP, which inhibits sodium reabsorption. If too much water is ingested solute concentration is
retained in the plasma and only water diuresis occurs. Finally, we see that acid-base balance is
regulated in the distal tubules and collecting ducts through type A and B intercalated cells.
Therefore, we were able to see the homeostatic mechanisms in the renal system, which was our
original purpose.
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V. References
1. Bautista E, Korber J. NPB 101L Systemic Physiology: Lab Manual. 2nd ed. Mason,
Ohio: Cengage Learning, 2009. Pgs 67-73
2. Sherwood, L. (2013). Human Physiology From Cells to System (8th ed.). Belmont,
California: Brooks/Cole. Pgs 505, 509, 514, 517, 522-523, 531-532, 537-541, 553-554,
556, 558-561, 570-573
3. Jensen, Janni M et al. Effect of Volume Expansion with Hypertonic- and Isotonic Saline
and Isotonic Glucose on Sodium and Water Transport in the Principal Cells in the
Kidney. BMC Nephrology 14 (2013): 202. PMC. Web. 18 Nov. 2016.
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Physiological Saline-A Quantitative Study-."Journal of Nutritional Science and
Vitaminology 52.5 (2006): 333-36. Web. 18 Nov. 2016
6. Murase, Takashi, Carolyn A. Ecelbarger, Erin A. Baker, Ying Tian, Mark A. Knepper, and
Joseph G. Verbalis. "Kidney Aquaporin-2 Expression during Escape from Antidiuresis Is
Not Related to Plasma or Tissue Osmolality." Journal of The American Society of
Nephrology 10 (1999): n. pag. Web. 18 Nov. 2016
7. Slatopolsky, Eduardo, Ivan O. Elkan, Carol Weerts, and Neal S. Bricker. "Studies on the
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