1. Integrative Physiology II: Fluid and Electrolyte Balance
Chapter 20
Integrative Physiology II: Fluid and Electrolyte Balance

2. Figure 20-3: Role of the kidneys in water balance
Body Water Balance
Urine concentration:
Dilute: 300 mOsM
Concentrated: 1200 mOsM
Figure 20-3: Role of the kidneys in water balance

3. What is “put back” and where in the nephron.
Proximal tubule
Glucose (those carriers) & Na+ (Primary active transport) urea (passive transport)
Loop of Henle
H2O and ions ( Na+, K+ & Cl-)
Distal tubule
Na+ & H2O
Collecting duct
H2O, Na+ & urea (again)

4. Overview: starts off isosmotic 300 mOsM (saltiness)
Figure 20-4: Osmolarity changes as fluid flows through the nephron

5. VASOPRESSIN: If we NEED water, we can get it from the collecting duct!

6. Vasopressin (a.k.a. ADH) regulates urine OsM: Let’s make concentrated uring part I
Figure 20-5: Water movement in the collecting duct in the presence and absence of vasopressin

7. Formation of Water Pores: Mechanism of Vasopressin Action

8. Figure 20-7: Factors affecting vasopressin release

9. Figure 20-10: Countercurrent exchange in the medulla of the kidney
Countercurrent exchanger. Loop of Henle Let’s make concentrated uring part II
Medullary osmotic gradient; more salty
Collecting duct
Figure 20-10: Countercurrent exchange in the medulla of the kidney

10. Why is it, countercurrent?
The players:
Loop of Henle
Descending/ascending
vasa recta
Ions: which ones?
H2O
Why is it, countercurrent?

11. Key facts:
1. descending LOH is water permeable, ascending LOH is NOT.
2. Ascending LOH actively pumps out ions.
3. water goes to where the most stuff is!!!
4. vasa recta removes water so it doesn’t dilute the medullary gradient.

12. SODIUM BALANCE:
What happens to the body’s OsM after eating salty fries? Increase/decrease
This triggers two responses; can you guess?

13. Vassopressin and thirst; both decrease OsM, but raise blood pressure.
To lower blood pressure our kidneys excrete sodium.
How does excreting sodium lower BP?

14. WATER GOES TO WHERE THE MOST STUFF IS.
When sodium leaves, water follows, decreasing ECF volume, and BP.

15. Sodium Balance: Intake & Excretion
Figure 20-11: Homeostatic responses to eating salt

16. Sodium is regulated by aldosterone from the adrenal cortex.
Aldosterone is actually secreted in response to blood pressure, blood volume and OsM.
More aldosterone: more sodium reabsorption.
Aldosterone target: principal cell (P cell) of the distal tubule & collecting duct.

17. Mechanism of Na+ Selective Reabsorption in Collecting Duct
!water does not follow!
Vassopressin must be present
Figure 20-12: Aldosterone action in principal cells

18. How does aldosterone get released
How does aldosterone get released? RAAS: renin-angiotensin-aldosterone-system
Figure 20-13: The renin-angiotensin-aldosterone pathway

19. Artial Natruretic Peptide: Regulates Na+ & H2O Excretion
Figure 20-15: Atrial natriuretic peptide

20. Potassium Balance: Critical for Excitable Heart & Nervous Tissues
Hypokalemia – low [K+] in ECF, Hyperkalemia - high [K+]
Reabsorbed in Ascending Loop, secreted in Collecting duct

21. Potassium Balance: Critical for Excitable Heart & Nervous Tissues
Figure 20-4: Osmolarity changes as fluid flows through the nephron

22. Potassium Balance: Critical for Excitable Heart & Nervous Tissues
Figure 20-12: Aldosterone action in principal cells

23. Integrative Physiology II: acid-base balance
Chapter 20, part B
Integrative Physiology II: acid-base balance

24. Acid/Base Homeostasis
Acidosis:  plasma pH
Protein damage
CNS depression
Alkalosis:  plasma pH
Hyperexcitability
CNS & heart
Buffers: HCO3- & proteins
H+ input: diet & metabolic
H+ output: lungs & kidney
Neutral pH is 7.0
Biological pH is 7.4
Determined based upon H+ concentration.

25. Acid/Base Homeostasis: Overview
Figure 20-18: Hydrogen balance in the body

26. Low pH – acidosis – nervous tissue becomes less exciteable – respiratory centers shut down.
High pH – alkalosis – neurons become hyperexciteable – twitching, numbness – tetenay and paralyzed respiratory muscles.

27. pH homeostasis depends on 3 things:
1. buffers
2. the lungs
3. the kidneys

28. Buffer systems Bicarbonate, phosphate ions, and proteins (Hb)
Buffers prevent significant changes in pH by binding or releasing H+
CO2 + H2O H2CO3 H+ + HCO3-
carbonic anhydrase

29. What will drive the equation to the right?
What will drive the equation to the left?
CO2 + H2O H2CO3 H+ + HCO3-
carbonic anhydrase
How can ventilation compensate for pH disturbances? Pg. 647.

30. Acidosis prevention at the Proximal Tubule: H+ excreted, bicarbonate reabsorption.
Na+ - H+ antiport activity
Glutamine metabolism
Figure 20-21: Proximal tubule secretion and reabsorption of filtered HCO3-

31. Kidney Hydrogen Ion Balancing: Collecting Duct
Type A Intercalated cells excrete H+ absorb HCO3-
Type B intercalated cells absorb H+ secrete HCO3-

32. Kidney Hydrogen Ion Balancing: Collecting Duct
The polarity of the two cells is reversed with the transport
proteins on opposite sides.
Figure 20-22: Role of the intercalated cell in acidosis and alkalosis

33. Acid-base disturbances: respiratory or metabolic
Respiratory acidosis –
hypoventilation & CO2 retention.
COPD- loss of alveolar tissue
Metabolic acidosis
Metabolic acids increase protons
Lactic acid from anaerobic metabolism burn sugar not oxygen.
Respiratory alkalosis
Hyperventilation rids CO2
Hysterical hyperventilation
Renal compensation can occur
Metabolic alkalosis
Vomiting stomach acids and taking bicarbonate-containing antacids.
Respiratory compensation takes place rapidly.