Renal 4: Volume/Pressure Regulation

Question 0

What do RBF and GFR stand for?

Answer 0

Renal Blood Flow and Glomerular Filtration Rate

Question 1

What’s the basic mechanism by which EC fluid is regulated?

Answer 1

The amount of Na+ excreted or absorbed

water follows sodium osmotically so changes in Na+ excretion - natriuresis - will alter water volume

Question 2

Describe autoregulation of GFR and RBF

Answer 2

Autoregulation is the control using local variables. Such as restricting the afferent arteriole (More??)

Question 3

What is Tubuloglomerular feedback?

Answer 3

Utilizes juxtaglomerular apparatus. Increased blood volume -> enhances tubular flow -> osmoreceptors in macula densa cells detect high levels of NaCl -> stimulate Na/K//Cl transporters -> macula densa cells release adenosine -> constricts afferent arteriole -> restore RBF and GFR (salt level!!! Not water)

Question 4

What is the myogenic mechanism?

Answer 4

Vascular smooth muscle contracts in response to stretch and dilates in response to low pressure (baroreceptors!)

Question 5

What 2 things influence the Starling forces that establish conditions for salt and water resorption?

Answer 5

1. Neuroendocrine mechanisms: Angiotensin II, aldosterone, sympathetic activity, ADH, natriuretic peptides.
2. Pressure natriuresis

Question 6

What is Renin?

Answer 6

A protease released from JGA cells that converts angiotensinogen to angiotensin I.

Question 7

What is ACE?

Answer 7

Angiotensin Converting Enzyme converts Angiotensin I to Angiotensin II

Question 8

Where is ACE found?

Answer 8

On pulmonary and renal endothelial cell surfaces

Question 9

What is the RAAS and what is it’s purpose?

Answer 9

Renin-Angiotensin-ADH-System. It promotes water and salt retention in response to a drop in BP

Question 10

What are Angiotensin II’s direct fast actions (1-2 minute half life)?

Answer 10

1. Constricts afferent arterioles to reduce RBF and GFR = less fluid out
2. Constricts efferent arterioles: decreases hydrostatic and increases oncotic pressures in capillaries = more fluid absorbed
3. Stimulates proximal tubule cells to reabsorb more Na+ and water

Question 11

What are Angiotensin II’s slower, indirect actions?

Answer 11

1. Releases aldosterone from the renal cortex
2. Releases ADH from the hypothalamus
3. Induces thirst from hypothalamus

Question 12

What is aldosterone?

1. trigger
2. source
3. action
4. time frame

Answer 12

A lipid soluble steroid hormone (a mineralcorticoid excreted by adrenal cortex)

• Increases Na+ reabsorption and K+ secretion
• Up-regs Na+/K+ ATPases, Na+ channels and ATP levels in principle cells
• Fine tunes Na+ levels
• slower production in adrenal cortex (up regulation), longer latency and longer duration.

Question 13

How does the efferent arteriole impact reabsorption?

Answer 13

CONSTRICTION = increased GFR and high tubular hydrostatic pressure; low vascular hydrostatic pressure, high vascular oncotic pressure: REABSORPTION of Na+ and water

DILATION = decreased GFR and low tubular hydrostatic pressure; high vascular hydrostatic pressure, low vascular oncotic pressure: EXCRETION of Na+ and water

Question 14

Differentiate gross from fine regulation in the neuroendocrine regulation of reabsorption

Answer 14

Gross: 67% of filtrate in proximal tubule is reabsorbed DESPITE changes in GFR via glomerular tubular balance.

Fine: reg of Na+ levels and EC volume is carried out by neuroendocrine control of Na+ reabsorption in both the proximal and distal portions of the tubule .

Question 15

What is the trigger of Angiotensin II?

Answer 15

A drop in blood pressure/volume (the Renin…etc)

Question 16

What is the source of Angiotensin II?

Answer 16

Angiotensin I, which derives from Angiotensinogen synthesized in the liver.

Question 17

What is the synthetic pathway of Angiotensin II?

Answer 17

Angiotensinogen converted by Renin into Angiotensin I; converted by ACE into Angiotensin II

Question 18

What is the action of Angiotensin II?

Answer 18

1. Vasoconstricts smooth muscle vasculature (afferent and efferent): increases resistance
2. Causes Na+ reabsorption in PROXIMAL tubule
3. Stimulates release of Aldosterone from adrenal cortex: reabsorp Na+ and water from DISTAL tubules
4. Stimulates release of ADH from pituitary in hypothalamus: Water (only) reabsorp from COLLECTING DUCTS
5. Induces thirst from hypothalamus: up intake

Question 19

What are the actions of Angiotensin II on renal vasculature and tubules.

Answer 19

Constricts afferent arterioles: reduce RBF and GFR (less fluid out)

Constricts efferent arterioles: decreases hydrostatic and increases oncotic pressures in capillaries (more fluid reabsorbed)

Reabsorption of water and salt from convoluted tubules and collecting duct

Question 20

What is the trigger and action of the sympathetic function in the kidney?

Answer 20

Trigger: drop is SYSTEMIC BP, emotional signals ie. fright

Action: baroreceptors detect drop, brain stem center activ symp neurons, postganglionic neurons innervate arterioles, JGA and tubular cells, release Renin …etc

Question 21

How does ADH fit into volume control?

Answer 21

It is an anti diuretic hormone that up regs aquaporins, allowing the reabsorption of water (w/out salt). Regulates osmoregulation, etc

Question 22

How does ANP inhibit reabsorption?

Answer 22

Atrial natriuretic peptides inhibits reabsorption by:

1. Increase GFR by dilating the afferent arteriole
2. Inhibit Na+ reabsorption by down reg Na+ channels
3. Inhibit H2O reabsorption by reducing ADH release
4. Inhibit secretion of renin and aldosterone

Question 23

How does pressure natriuresis inhibit reabsorption?

Answer 23

Increase BP, more blood thru sys pushes out on vessel walls, shear stress causes release of NO, vessels dilate, altering g starling forces, gradient is not as steep, less reabsorption, more excretion!!

Question 24

What is the relationship between pressure natriuresis and NO?

Answer 24

The increased pressure of the blood flow causes shear stress on vessel walls, causing NO release: vasodilator a vasa recta, increases capillary hydrostatic pressure which inhibits Na+ and water reabsorption

Question 25

When is ANP and the other natriuretic peptides released, and what for?

Answer 25

In response to increased blood volume or pressure; work to reverse actions of RAAS