Ansari, 1

Renal System Homeostasis of

ECF Volume, Osmolarity, and

Acid-Base Balance
By Sidra Ansari November 22, 2016

Lab Partners:

Benjamin Van

Yvonne Lee

Skyler Suchovsky

Lab TA: Michael Fong

 Ansari, 2

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

is urine along with waste. (Sherwood, 2013)

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
 Ansari, 3

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

in the discussion of the lab (Sherwood, 2013).

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)
 Ansari, 4

II. Materials and Methods

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
 Ansari, 5

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

calculate the sodium clearance rate.

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.
 Ansari, 6

III. Results

For all graphs a urine sample was not collected at Time = 120 minutes for the alkalosis

subject.

Time Vs. Flow Rate

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
 Ansari, 7

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

In order to estimate GFR, we calculated creatinine clearance and plotted it on a

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
 Ansari, 8

187 ml/min to 126 ml/min. Meanwhile, the controls creatining clrance rate did not

significantly and was stable around 160 ml/min.

Sodium Concentration and Sodium Clearance.

In order to calculate sodium clearance, the sodium concentration of the urine

samples was measured. As seem in Figure 3, the hypotonic subject experienced a

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

constant sodium concentration around 85 mEq/L.

 Ansari, 9

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

and stayed around 0.3 ml/min.

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
 Ansari, 10

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

specific gravity decreases to 1.0009 before increasing to 1.0144. In the hypotonic

subject, the specific gravity decreased from 1.0237 to 1.000 between 0-90 minutes,

before increasing to 1.009 at 120 minutes.

Urine pH
 Ansari, 11

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

Figure 6: Overall increase in We

pH were
for bicarbonate subjecta half ansample
hour after ingestion
increases from 6.83 to 7.77. unable to collect urine for T=120 butofit

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.
 Ansari, 12

Water/Sodium Excreted Expected Vs. Actual

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

Table 1: Expected water volume/sodium secretion vs. actual water volume/sodium

secretion; Isotonic and hypotonic subjects secreted more water than expected;
Isotonic subject secreted slightly less sodium than expected while hypotonic subject
secreted significantly less sodium than expected

Water and Sodium Excretion Values

Control Isotonic Hypotonic Alkalosis
Water Expected 64.8 148 106 699
(ml)
Water Actual 59 446 502 102
(ml)
Sodium Expected 0.1353 0.5984 0.2528 0.4680
(g)
Sodium Actual 0.1166 0.5833 0.09662 0.2481
(g)

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.
 Ansari, 13

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

concentration and pH.

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,

sodium clearance and specific gravity.

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
 Ansari, 14

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

hypothesis of increased flow rate in hypotonic subjects due to hypervolemia.

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

normally released by angiotensin II stimulation through the RAAS system in response to a

decrease in ECF. It then recruits AQP-2, aquaporins or water channels, to the cell surface and
 Ansari, 15

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
 Ansari, 16

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

concentration (microliters/min) was observed (Atherton 1970). In another experiment, uremic

patients were infused with hypotonic solution and still exhibited an increase in GFR due to the

volume expansion (Slatopolsky, 1968).

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

and physiology do support our hypothesis.

 Ansari, 17

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

urine). We hypothesized that there would be an increase in urinary sodium concentration,

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.

In Figure 3, we see that sodium concentrations in the isotonic subject fluctuated by

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.
 Ansari, 18

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

increase in urinary sodium concentration, sodium clearance and specific gravity.

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
 Ansari, 19

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

increase reabsorption of sodium and thus water (Sherwood, 2013).

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

by our results and by research.

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
 Ansari, 20

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

and supported the above studys results (Cohen et at., 2013).

An increase in urinary pH is seen following ingestion of bicarbonate due to the actions of

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
 Ansari, 21

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

alkalosis and maintain acid-base balance (Sherwood, 2013) Page 571-573.

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

through decreased secretion of vasopressin. ECF osmolarity is maintained by either excreting

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.
 Ansari, 22

V. References

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Ohio: Cengage Learning, 2009. Pgs 67-73
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556, 558-561, 570-573
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 Ansari, 23

8. Kougias, Panagiotis et al. Arterial Baroreceptors in the Management of Systemic

Hypertension. Medical science monitor: international medical journal of experimental
and clinical research 16.1 (2010): RA1RA8. Web. 19 Nov. 2016
9. Udokang, N.E., and B.A. Akpogomeh. "Effect of Volume Loading with Water Normal
Saline Palm Wine and Lipton Tea on Urinary Output, PH, Specific Gravity, Sodium and
Potassium Concentrations in Human Subjects." Nigerian Journal of Physiological
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