8. Control Of Plasma Osmolarity

Question 1

Where are osmoreceptors located?

Answer 1

In the OVLT of the hypothalamus.

Question 2

How do osmoreceptors sense changes in plasma osmolarity?

Answer 2

Via fenestrated leaky endothelium exposed directly to systemic circulation.

Question 3

What two secondary responses are mediated via two pathways triggered by increased plasma osmolarity detection by osmoreceptors?

Answer 3

Concentration of urine (ADH).

Increased water intake (thirst).

Question 4

What anatomical relationship allows the OVLT to stimulate the production of ADH?

Answer 4

Lies close to the supraoptic nucleus of hypothalamus (where ADH is made), with input from baroreceptors.

Question 5

When there are changes in blood volume and osmolarity, which is conserved by the body preferentially?

Answer 5

Plasma volume.

Question 6

What is the analogue of thirst?

Answer 6

Salt ingestion.

Question 7

What are the two types of salt appetite?

Answer 7

Hedonistic appetite.

Regulatory appetite.

Question 8

How much of a change in plasma osmolarity is needed to stimulate ADH release?

Answer 8

1% increase.

Question 9

How much of a change is plasma osmolarity is needed to stimulate the thirst response?

Answer 9

Increase in osmolarity of 10% (or decrease in volume).

Question 10

Where is ADH released from?

Answer 10

Posterior pituitary.

Question 11

What does ADH increase the permeability of the collecting duct to help control osmolarity?

Answer 11

Water and urea.

Question 12

What condition results from plasma ADH levels being too low?

Answer 12

Central (ADH release affected) Diabetes Insipidus.

Question 13

What conditions results from acquired kidney insensitivity to ADH?

Answer 13

Nephrogenic diabetes insipidus.

Question 14

How would you manage diabetes insipidus clinically?

Answer 14

ADH injections or ADH nasal spray treatments.

Question 15

Give 2 pathologies that can result in plasma ADH levels being too low.

Answer 15

Damage done to hypothalamus or pituitary
gland.
A brain injury, particularly a fracture of the base of the skull.
A tumour.
Sarcoidosis or tuberculosis.
An aneurysm.
Some forms of encephalitis or meningitis.
The rare disease Langerhans cell histiocytosis

Question 16

What conditions results form excessive release of ADH from the posterior pituitary gland or another source?

Answer 16

Syndrome of inappropriate antidiuretic hormone secretion (SIADH).

Question 17

What happens to plasma sodium levels and total body fluid in increased ADH release?

Answer 17

Dilutional hyponatraemia in which the plasma Na+ levels are lowered and total body fluid is increased.

Question 18

What happens to aquaporin expression in the kidneys if plasma osmolarity decreases?

Answer 18

No ADH stimulation, no AQP2 in apical membrane, AQP3 and AQP4 on basolateral membrane only in the latter distal convoluted tubule and collecting ducts. Diuresis.

Question 19

What happens to aquaporin expression in the kidneys if plasma osmolarity increases?

Answer 19

ADH release, insertion of AQP2 channels into the apical membrane of the collecting duct, to increased water reabsorption (needs a hypertonic interstitium).
Hyperosmotic urine produced.

Question 20

What is the medullary counter current mechanism?

Answer 20

The entire functional organisation in the medulla to result in the concentration of urine.

Question 21

What 4 mechanisms make up the medullary counter current mechanism?

Answer 21

Juxtamedullary nephron – long loop of Henle establish (create) the vertical osmotic gradient.
Vasa recta help to maintain (preserve) this osmotic gradient.
Collecting duct of all nephrons use the gradient along with hormone ADH (vasopressin) to produce urine of varying concentration.
Urea also helps in urine concentration mechanism.

Question 22

What features of the loop of Henle lead to counter current multiplication?

Answer 22

Descending limb is highly permeable to water due to AQP1, but not permeable to Na+.
Ascending limb actively transports NaCl out of the tubular lumen into the interstitial fluid, but is impermeable to water.
So the interstitial fluid is isotonic at the corticomedullary border, and the medullary interstitium is hyperosmotic at the papilla.

Question 23

What is an effective osmole?

Answer 23

Solutes which are not able to freely cross the nephron membrane, making them able to exert an osmotic force across the membrane. Eg urea.

Question 24

What happens in the recycling of urea?

Answer 24

Cortical collecting duct cells are impermeable to urea. ADH causes the insertion of urea channels into the collecting duct, so that urea is reabsorbed (helps water to also be reabsorbed). The urea then moves into the interstitium and diffuses back into the loop of Henle.

Question 25

What is the maximum osmolarity at the tip of the loop of Henle?

Answer 25

1200 mOsm/Kg.

Question 26

The concentration gradient in the kidney is produced by the loop of Henle acting as a counter current multiplier, but what maintains it?

Answer 26

The vasa recta acting as a counter-current exchanger.

Question 27

What feature of vasa recta blood flow allows the osmotic gradient to be maintained?

Answer 27

Blood flow in the vasa recta is in the opposite direction to fluid flow in the tubule.

Question 28

Describe what happens in the descending and then ascending limb of the vase recta?

Answer 28

Isosmotic blood in vasa recta enters hyperosmotic milieu of the medulla ( high conc. Na+ ions, Cl- ions and urea). Na+, Cl- and urea diffuse into the lumen of vasa recta. The osmolarity of the blood in vasa recta increases as it reaches tip of hairpin loop.
Blood ascending towards cortex will have higher solute content than surrounding interstitium and so water moves in from the descending limb of the loop of Henle.

Question 29

Why does blood flow slowly through the vasa recta?

Answer 29

Lower total plasma blood flow (5-10% of RPF), but still needs to deliver nutrients and maintain medullary hyper-tonicity.