1. Regulation of Extracellular Fluid Osmolarity and Sodium Concentration

2. Excretion of excessive water by forming a dilute urine
The kidneys can excrete urine with an osmolarity as low as 50 mOsm/L (1/6 of normal urine osmolarity)
Conversely, when there is a deficit of water and extracellular fluid osmolarity is high, the kidney can excrete a urine with osmolarity as high as mOsm/L
Role of anti-diuretic hormone (Vasopressin) in concentrating urine

3. Renal Mechanisms for Excreting a Dilute Urine

4. Generating a dilute urine
from: Guyton, AG & Hall, JE, Medical Physiology (10th Ed.), 2000, Chp. 28.
A dilute urine results from the reabsorption of salt from tubule segments
impermeable to H2O.

5. Tubular Fluid Becomes Dilute in the Ascending Loop of Henle

6. Excretion of Concentrated Urine
Ability of the kidney to form a more concentrated urine is essential for survival
It is achieved by increased water reabsorption and increased solute excretion
Obligatory urine volume
A normal adult must excrete about 600 mOsm of solutes per day
If the maximal urine concentration ability is 1200 mOsm/L, the minimal volume of urine that must be excreted:
600 mOsm L/ 1200 mOsm L = 0.5 L/ Day

7. Requirements for excreting a concentrated urine
High ADH levels
Hyperosmotic renal medulla which provides the osmotic gradient necessary for water reabsorption to occur in the presence of high levels of ADH

8. Generating a concentrated urine
A concentrated urine results from the reabsorption of H2O (by osmosis)
from tubule segments that are exposed to a hyperosmotic interstitium.

9. Requirements for excreting a concentrated urine
Major factors that contribute to the buildup of solute concentration in the renal medulla:
Active transport of Na ions and co-transport of K, Cl and other ions out of the thick portion of Henle
Active transport of ions from the collecting ducts into the medullary interstitium
Facilitated diffusion of urea from the medullary collecting ducts into the medullary interstitium
Diffusion of only small amounts of water from the medullary tubules into the medullary interstitium

10. Countercurrent Mechanism Produces a Hyperosmotic Renal Medullary Interstitium

11. Countercurrent Mechanism Produces a Hyperosmotic Renal Medullary Interstitium
Countercurrent multiplication
Between ascending and descending limbs of loop
Creates osmotic gradient in medulla
Facilitates reabsorption of water and solutes before the DCT
Permits passive reabsorption of water from tubular fluid

12. Role of distal tubule and collecting ducts in excreting a concentrated urine

13. Urea Contributes to Hyperosmotic Renal Medullary Interstitum and to a Concentrated Urine

14. Preservation of Hyperosmolarity by Vasa Recta
1) Medullary blood flow is low
2) The vasa recta serves as countercurrent exchangers
The vasa recta does not create the hyperosmolarity, but they do prevent it from being washed away

15. The vasa recta The vasa recta are hairpin- shaped vessels that run
parallel to the loop of Henle.

16. Urine Concentration Mechanism

17. Changes in osmolarity of tubular fluid

18. Disorders of Urinary Concentrating Ability
1) Inappropriate secretion of ADH
2) Impairement of countercurrent mechanism
3) Inability of the distal tubule, collecting tubule and collecting ducts to respond to ADH
Failure to produce ADH (Central diabetes insipidus)
Inability of the kidneys to respond to ADH (Nephrogenic diabetes insipidus)

19. Control of Water Absorption by ADH

20. Control of Extracellular Fluid Osmolarity and Na Concentration
Osmoreceptor – ADH feedback system

21. ADH Synthesis in Supraoptic and Paraventricular Nuclei of the Hypothalamus and ADH release from the posterior pituitary

22. Decreased arterial pressure and / or blood volume
Cardiovascular reflex stimulation of ADH release by decreased Arterial Pressure and/or decreased blood volume
Decreased arterial pressure and / or blood volume
Arterial baroreceptor reflexes
Cardiopulmonary reflexes
Increase ADH
Decrease ADH
↑ Plasma osmolarity
↓ Plasma osmolarity
↓ Blood volume
↑ Blood volume
↓ Blood pressure
↑ Blood pressure
Nausea
Hypoxia
Drugs:
  Morphine
  Alcohol
  Nicotine
  Clonidine (antihypertensive drug)
  Cyclophosphamide
  Haloperidol (dopamine blocker)

23. Role of Thirst in Controlling Extracellular Fluid Osmolarity and Sodium Concentration
CNS centers for thirst – hypothalamus – anteroventral wall of the 3rd ventricle
Stimuli for thirst: increased extracellular fluid osmolarity
Salt-apetite mechanism for controlling extracellular fluid Na concentration and volume
There are two primary stimuli to increase salt apetite:
Decreased extracellular fluid Na concentration
Decreased blood volume or blood pressure associated with circulatory insufficiency

24. Control of Extracellular Fluid Sodium Concentration: ADH and Thirst