Met 2: Nephro; Lec. 2 Integration Of Salt And Water Balance

Front 1

What percentage of our total body weight is water? How is this water distributed (compartment-wise)?

Back 1

60% (males), 50% (females)

40% - intracelluar fluid (or 2/3 of water)
20% - extracellular fluid (or 1/3 of water)

only force at play at the cell membrane is osmotic gradient

Front 2

What are the divisions of fluid in the ECF?
And the main force?

Back 2

Interstitial fluid (3/4 of ECF)
Plasma (1/4 ECF)

movement across the capillary wall depends on water gradients and hydrostatic gradients

Front 3

What is the main cation in the extracellular fluid (ECF) compartment? The intracellular fluid (ICF) compartment?

Back 3

ECF: Sodium - Na+

ICF: Potassium (K+)

Front 4

Can you change the amount of ICF Na?

Back 4

No. The Na/K pump regulates this

Front 5

"What is the formula for osmotic concentration?

Ex: What is the osmotic concentration of 100 M NaCl?"

Back 5

Osmotic concentration = {# of dissociated particles} x [solute]

Ex: 200 M - because NaCl dissociates into 2 particles

Front 6

What will happen to a cell in a solution of 290 mOsm/L? In a solution of 360 mOsm/L? In a solution of 200 mOsm/L?

Back 6

This is based on normal sodium concentration of 145 mEq/L.

A) No change (isotonic solution)
B) Cell shrinks, exodus of water (hypertonic solution)
C) Cell expands, influx of water (hypotonic solution)

Front 7

How is water lost to maintain water balance?

(Fill in the arrows above)

Back 7

"1) Insensible losses (i.e. losses we can't regulate) - evaporation, respiration

2) Sweat and feces

3) Urine (primary source of water loss)"

Front 8

What is meant by the "minimum urine volume"?

Back 8

"The minimum amount of urine the kidneys have to produce in order to remove all the waste products. If you go below the minimum output, you are considered to be in renal failure.

In lecture, he gave an example of 500 mL."

Front 9

What occurs physiologically when there is an increase in plasma osmolality (ex. during dehydration)? Where are the sensors located?

Back 9

1) The thirst centre will be triggered

2) ADH release, triggering water reabsorption

The osmoreceptors are located within the hypothalamus.

Front 10

Where is ADH produced and how is its release regulated?

Back 10

Two clusters of neurons (supraoptic and paraventricular) in the hypothalamus are responsible for the production of ADH.

Their axons terminate within the posterior pituitary, where they are released. Its release is regulated by osmoreceptors and in part by baroreceptors.

ADH is released at 280 normal osmolarity is 290, so there is always circulating ADH

Front 11

What has to happen for baroreceptors to stimulate the release of ADH?

Back 11

There must be a decrease in circulating volume (drop in blood pressure) to stimulate ADH release to restore circulating volume.

Front 12

What sets up the osmotic gradient in the distal tubule (i.e. the cortex) that allows ADH to stimulate water reabsorption?

Back 12

The sodium reabsorption in the ascending loop of Henle and the early distal tubule (both water impermeable) results in a concentrated area in the interstitial environment

Once ADH is present and water channels open, there is an osmotic gradient present and water reabsorption follows.

Front 13

What sets up the osmotic gradient in the collecting duct (i.e. the medulla) that allows ADH to stimulate water reabsorption?

Back 13

1) The sodium transport that occured in the loop of Henle, increasing the osmolarity of the interstitial environment.

2) The addition of urea by the inner medullary collecting duct.

These both create a large concentration gradient, allowing water to be reabsorbed in the presence of ADH.

Front 14

what are the responses to dehydration and excess hydration

Back 14

Front 15

How would any acute increases in sodium intake affect the kidney?

Back 15

There would be an increase in sodium excretion by the kidneys, but the response would be much more sluggish (days) than that of a water-ADH repsonse.

ECF volume would increase, along with body weight.

Front 16

Describe edema in terms of changes in ECF

Back 16

There is not an actual change in the overall amount of ECF instead there is only a change in the ratio of volume from the vascular compartment to the interstitial compartment

Front 17

How does the kidney know when to increase or decreases sodium excretion?

Back 17

Based on baroreceptors sensing circulating volume located in cardiovascular organs. The baroreceptors stimulate the SNS, which has a direct effect on the level of sodium excretion within the kidneys. Effects are to increase reabsorption of Na at the PCT

The SNS also stimulates the renin - angiotensin - aldosterone system.

Front 18

Describe the production of angiotensin II.

Back 18

1) Low blood volume stimulates renin release from the kidney.

2) Circulating angiotensinogen from the liver is converted to angiotensin I by renin. Angiotensin I has no physiological function.

3) Angiotensin I is converted by angiotensin converting enzyme (ACE) in capillary networks (primarily in the lungs) to angiotensin II

Front 19

What are the physiological effects of angiotensin II?

Back 19

1) Vasoconstriction targeting blood vessels to increased blood pressure.

2) Acts on the hypothalamus to increase thirst and through ADH release, stimulating water reabsorption.

3) Acts on the proximal tubules of the kidney directly to stimulate the reabsorption of sodium. NA/H pump

4) Acts on the adrenal cortex to release aldosterone and increase sodium reabsorption by the late distal tubule and collecting duct.

Front 20

What are four means at which the body maintains appropriate renin levels?

Back 20

1) Systemic baroreceptors within blood vessels. which will adapt and therefore lose effect over time

2) Intrarenal baroreceptors within the kidney. Don't adapt

3) NaCl levels within the tubular fluid of the macula densa in the distal tubule.

4) Product inhibition of circulating angiotensin II (negative feedback)

Front 21

What are two pharmacological means of regulating circulating angiotensin II levels?

Back 21

1) ACE inhibitors - target the converting enzyme

2) AT1 receptor blockers - block receptors on the proximal tubule cells, reducing the effects of circulating angiotensin II levels.

Front 22

What hormone allows the kidney to get rid of excess fluid?

Back 22

Atrial natriuretic peptide (ANP) - released by the muscle cells within the atria of the heart.

Front 23

How does atrial natiuretic peptide work?

Back 23

1) It is a powerful vasodilator, targeting the afferent arteriole, leading to an increased GFR and sodium and water excretion.

2) It targets sodium transport, inhibiting sodium reabsorption in the distal tubule and collecting duct.

3) It blocks ADH and renin release and interferes with aldosterone release, hormones that normally increase sodium and water retention.

Front 24

overview of response to volume depletion

Back 24

Front 25

Overview of response to volume expansion

Back 25