Exam #4: Renal Hormones & Autacoids Flashcards Preview

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Flashcards in Exam #4: Renal Hormones & Autacoids Deck (37)
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1
Q

Describe the two intrinsic renal mechanism for autoregulation of renal blood flow (RBF) & glomerular filtration rate?

A

1) Myogenic mechanism= blood vessels resist stretching by contracting in response to increased wall tension i.e. pressure; there is also a reflexive vasodilation in response to decreased wall tension/ stretch
- In the nephron, increased pressure in afferent arteriole= contraction, and prevention of increased hydrostatic pressure in the glomerulus

2) Tubuloglomerular feedback mechanism

2
Q

Describe tubuloglomerular feedback for control of GFR and NaCl delivery to the distal tubule.

A

1) Increased renal a. pressure= increased GFR & RBF
2) Increased tubular fluid flow
3) Increased flow= less NaCl reabsorption in proximal tubule, b/c less time for reabsorption
4) Eventually, macula densa senses increased flow & NaCl concentration
4) Macula densa secretes ADENOSINE that causes VASOCONSTRICTION of the afferent arteriole

*Note that this effect of adenosine in the kidney is opposite of its normal effect

3
Q

What is the role of the macula densa?

A

1) Sense increased flow & NaCl concentration
2) Secretion of ADENOSINE that causes VASOCONSTRICTION of the afferent arteriole
3) Inhibition of Renin release–>decrease systemic blood pressure

4
Q

How can tubuloglomerular feedback help prevent excessive fluid losses if there is damage to kidney proximal tubules?

A

Similar mechanism to increased GFR & RBF, there is LESS water and NaCl sensed at the macula densa–>vasoconstriction of the afferent arteriole to prevent excessive fluid loss from damaged nephrons

5
Q

Give proposed reason why autoregulation is useful.

A

1) Many activities alter BP, want to uncouple BP from GFR & RBF to keep them CONSTANT
2) Prevent changes in urine output and electrolyte balance based on acute blood pressure changes

6
Q

Can autoregulation still protect the kidney in patients with severe systemic hypertension?

A

No, these mechanisms stop working at the extremes of blood pressure, but very low and very high

7
Q

Give the names of the autacoids/hormones which can vasodilate the afferent and efferent arterioles.

A

Vasodilator prostaglandins, PGE2 & PGI2 (prostacyclin)

8
Q

Which hormones/autacoids cause vasoconstriction?

A

Angiotensin II
NE
Vasopressin (ADH)
Endothelin

9
Q

Explain why drugs that inhibit prostaglandin synthesis can cause renal damage.

A

Reduced amounts of PGE2 & PGI2 leave vasoconstriction unopposed and can lead to renal damage

10
Q

What common drugs that inhibit prostaglandin synthesis?

A

NSAIDs e.g. ASA, ibuprofen, naproxen

*****Note that patient’s with chronic renal disease should NOT take NSAIDs–compensatory increase in single nephron GFR is maintained by prostaglandins; knock these out–> immediate renal failure

11
Q

Outline the renin-angiotensin-aldosterone system. Where is each produced?

A

p. 163

Renin= juxtaglomerular cells of the kidney 
Angiotensinogen= liver 
ACE= lungs and kidneys 
Angiotensinogen II= lung and kidneys 
Aldosterone= adrenal cortex
12
Q

State which cells produce most renin and how renin release is controlled.

A

Renin is produced by juxtaglomerular cells of the kidney and is secreted in response to decrease arterial pressure, and B1 stimulation

13
Q

Which division of the autonomic nervous system innervates the cells that produce renin?

A

Stimulation of B1 adrenergic receptors

14
Q

Outline the pathway from angiotensinogen to angiotensin II.

A

Angiotensin I is converted into Angiotensin II via Angiotensin Converting Enzyme (ACE)

15
Q

Where do renin and angiotensin converting enzyme (ACE) act in this pathway (angiotensinogen to angiotensin II)?

A

Lung & kidney

16
Q

Describe the effect of angiotensin II on the vascular smooth muscles.

A

Angiotensin II causes vasoconstriction of vascular smooth muscle

17
Q

Describe the effect of angiotensin II on the adrenal cortex.

A

Angiotensin II increases secretion of aldosterone from the adrenal cortex

18
Q

Describe the effect of angiotensin II on the efferent arteriole.

A

In the kidney, angiotensin II preferentially vasoconstricts the efferent arteriole b/c of the vasodilator prostaglandins and NO that act on the afferent arteriole

19
Q

Describe the effect of angiotensin II on the proximal tubule Na+ reabsorption.

A

Increases the activity of the Na+-H+ exchanger to increase Na+ retention (and consequently, water retention)

20
Q

Describe the effect of angiotensin II on the thirst center.

A

Increases thirst

21
Q

Describe the effect of angiotensin II on the release of ADH .

A

Increases secretion of ADH

22
Q

Describe the effect of angiotensin II on sympathetic tone.

A

Increases sympathetic tone

23
Q

State the two main sources of erythropoietin production. Which organ makes the most (~90%) erythropoietin?

A

1) Kidney= majority of EPO synthesis

2) Liver

24
Q

What is the effect of erythropoietin on RBC production?

A

EPO increases RBC production

25
Q

What are the major stimuli for erythropoietin secretion?

A

Kidney senses oxygen levels and secrets EPO when oxygen levels drop

26
Q

Describe the role of the kidney in making the active form of vitamin D.

A

Generally, the kidney is responsible for the last step of Vitamin D synthesis

  • Vitamin D3 is converted to 25-hydroxycholecaliferol in the liver
  • In the kidney, it is converted to 1,25-dihydroxy vitamin D, or Calcitrol
27
Q

What is the major action of the active form of vitamin D? (What is its effect on the intestine? On the kidney? Which effect is more important?)

A

Intestine= increase absorption of Ca++ & phosphate*

Kidney= increased reabsorption of Ca++ & phosphate

*****Note that the action of Vitamin D in the intestine is more important that the same effect in the kidney

28
Q

Describe the effect of parathyroid hormone on the kidney.

A
  • Formation of the active form of Vitamin D (Calctriol) is stimulated by PTH action on the kidney
  • INCREASES Ca++ reabsorption in the kidney but DECREASES reabsorption of phosphate (vs. Calcitriol that increases absorption of both)
29
Q

Describe how chronic renal failure affects the patient’s bones.

A
  • Chronic renal failure= low GFR & increased plasma phosphate
  • Elevated phosphate increases PTH
  • PTH causes bone resorption

–> “Renal Osteodystrophy”

30
Q

Describe the effects of constricting either the afferent or the efferent arteriole on renal blood flow (RBF).

A
Afferent= decrease RBF 
Efferent= decrease RBF
31
Q

Describe the effects of constricting either the afferent or the efferent arteriole on GFR.

A
Afferent= decreased GFR 
Efferent= increased GFR
32
Q

How could you increase the glomerular hydrostatic pressure by constricting the efferent or afferent arterioles?

A

Constricting the efferent arteriole

33
Q

What is the source of fibroblast growth factor 23 (FGF 23).

A

Osteoblasts and osteocytes in bone

34
Q

What is FGF23?

A

“fibroblast growth factor 23”

35
Q

What are the effects of FGF23 on the kidney?

A

1) Decreased reabsorption of phosphate

2) Decreases the production of calcitriol

36
Q

What stimulates the secretion of FGF23?

A

1) Elevated phosphate levels

2) Calcitriol i.e. active Vitamin D

37
Q

What are the relationships between FGF23 and parathyroid hormone and calcitriol and their actions?

A

Vitamin D= increased reabsorption of Ca++ & phosphate

FGF23= decreased reabsorption of Ca++ & phosphate

PTH= increased absorption of Ca++. decreased absorption of phosphate

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