Lecture 2: Regulation of Na+ and H2O Balance

Question 1

What is released by the kidneys that stimulated RBC production and affects blood volume?

Answer 1

Erythropoietin

Question 2

Neurons responsive to changes in osmolality; activation causes release of?

Answer 2

Osmoreceptors; release of ADH

Question 3

How sensitive are the osmoreceptors?

Answer 3

VERY sensitive, respond to change of 1 or 2 mOsm/kg

Question 4

When osmoreceptors are faced with hyperosmolality, what happens?

Answer 4

Release of ADH, preventing further loss of water in urine, and stimulates thirst.

Question 5

What molecules have the largest affect on the stimulation of ADH (vasopressin) secretion and thirst; which sugars via which method?

Answer 5

• Na+

- Sugars such as mannitol and sucrose when infused IV

Question 6

How do increases in plasma osmolality caused by urea and glucose affect the secretion of plasma ADH levels?

Answer 6

Urea and glucose have little or no affect

Question 7

What do arterial baroreceptors do?

Answer 7

Sense changes in the aorta and carotid arteries, sending afferent information to the brainstem vasomotor center, which then regulates CV and renal processes via autonomic efferents

Question 8

How do cardiopulmonary baroreceptors work?

Answer 8

• Sense pressure in the cardiac atria and pulmonary arteries.
• Send afferent info in parallel w/ the arterial baroreceptors

Question 9

There is some overlap in the cardiopulmonary and arterial baroreceptors, but which are the most important for ADH?

Answer 9

Cardiopulmonary baroreceptors have important influence on the hypothalamus, which regulates secretion of ADH

Question 10

The binding of ADH to the V2 receptors causes what?

Answer 10

• Stimulates a Gs-coupled protein that activates adenylyl cyclase, in turn causing production of cAMP to activates Protein Kinase A
• Increases aquaporin-2 channel formation and apical membrane insertion, increasing H2O permeability of the collecting duct

Question 11

How do the cortical collecting ducts compare to the medullary collecting tubules in regards to permeability?

Answer 11

Cortical collecting ducts - permeable to H2O at all times

Medullary - determined by the secretion of ADH, which is controlled by response of hypothalamic osmoreceptors

Question 12

What is the major stimulus for ADH (vasopressin) secretion and thirst; what’s another stimulus?

Answer 12

• Increased ECF osmolarity (MAJOR)

- Decreased ECF volume (important for large changes in ECF volume/arterial BP)

Question 13

The 2 cells of the JGA and their role?

Answer 13

1) Macula densa - the sensor!

2) Juxtaglomerular cells - secrete renin

Question 14

If Na+ is high and fluid volume is low, what 2 things do the macula densa do?

Answer 14

1) Tell juxtaglomerular cells to release renin

2) Dilate the AFFERENT arteriole of the glomerulus (by secreting a little ADH)

Question 15

The juxtaglomerular cells secrete renin in response to what 3 things?

Answer 15

1) Beta-adrenergic stimulation (sympathetics)
2) Decreases renal perfusion (in afferent arterioles - decreased glomerular hydrostatic pressure)
3) Signals from Macula Densa

Question 16

What is the primary and secondary effects of the RAAS system?

Answer 16

Primary - maintain systemic BP

Secondary - Preserves the GFR

Question 17

How does renin contribute to maintaining GFR?

Answer 17

• Renin converts angiotensinogen to angiotensin I, which is then converted by ACE to angiotensin II
• Angiotensin II promotes vasoconstriction of efferent arterioles which increases GFR

Question 18

Angiotensin II promotes vasoconstriction of?

Answer 18

• Efferent arterioles = raises glomerular hydrostatic pressure
• All renal blood vessels and systemic vessels

Question 19

Angiotensin II works to increase reabsorption of what, in which part of the kidney?

Answer 19

Reabsorption of Na+ and Cl- from the proximal tubule, in turn causing reabsorption of water.

Question 20

Aldosterone is released from where in response to what?

Answer 20

• Released from Adrenal Cortex

- Increased plasma K+, decreased plasma Na+, or decreased BP

Question 21

Where does aldosterone act?

Answer 21

Thick segment of the nephron loop, DCT, and cortical portion of collecting duct

Question 22

A rise in plasma K+ stimulates the adrenal cortex to?

Answer 22

Increase its output of aldosterone, which in turn promotes the secretion and ultimate excretion/elimination of excess K+

Question 23

The net effect of aldosterone is?

Answer 23

Conserve and increase water levels in the plasma by reducing the excretion of Na+, and thus water, from the kidneys

Question 24

When osmolality of ECF increases what occurs to aldosterone?

Answer 24

A negative feedback loop will inhibit the release of aldosterone.

Question 25

How does RAAS cause increased angiotensin

Answer 25

Angiotensin II promotes the release of Aldosterone from the adrenal cortex

Question 26

What system opposes RAAS?

Answer 26

Blood pressure lowering system that involves - Atrial Natriuretic Peptide (ANP)

Question 27

Where is ANP produced and what does it promote?

Answer 27

Produced in atrial cardiac muscle cells and promote excretion of large amounts of Na+ in the urine

Question 28

The main action of ANP is what and happens in what part of the nephron?

Answer 28

Directly inhibit Na+ reabsorption in the distal parts of the nephron, thus increasing Na+ excretion and accompanying osmotic H2O excretion in urine

Question 29

What 2 things does RAAS inhibit?

Answer 29

1) Inhibits renin secretion by the kidneys and acts on the adrenal cortex to inhibit aldosterone secretion
2) Inhibits secretion and actions of ADH

Question 30

What affect does ANP have on the smooth muscle of afferent arterioles?

Answer 30

Inhibits them causing relaxation (vasodilation) and increasing GFR —> Increases Na+ and H2O filtration

Question 31

Hyponatremia describes a state where?

Answer 31

• Plasma Na+ concentration is lower than normal

- Body fluids are diluted and cells swell from decrease osmolality

Question 32

What is a consequence of hyponatremia?

Answer 32

Cerebral edema and hypovolemia

Question 33

SIADH causes excessive release of what, leading to?

Answer 33

Excessive ADH, leading to excessive H2O retention, cells swell, and increased Na+ secretion (major cause of low Na+ levels)

Question 34

What causes:

urine > serum osmolality
serum > urine osmolality?

Answer 34

Urine > Serum = SIADH

Serum > Urine = Water intoxication

Question 35

What is the difference between nephrogenic and central diabetes insipidus?

Answer 35

Central: Decreased secretion of ADH

Nephrogenic: Kidney resistance to ADH

Question 36

The administration of ADH will, in moderate to severe cases raise urine osmolality and lower the urine volume by more than 50% in which kind of diabetes insipidus?

Answer 36

Central Diabetes Insipidus

Question 37

Causes of central diabetes insipidus?

Answer 37

1) Head trauma
2) Pituitary tumor
3) Neurosurgery

Question 38

Causes of nephrogenic diabetes insipidus?

Answer 38

1) Lithium toxicity
2) Renal disease
3) Hypokalemia
4) Pregnancy