Renal Regulation of ECF Volume and Diuretics Flashcards

1
Q

osmoreceptors are located in the

A

hypothalamus

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2
Q

baroreceptors are located in the

A

afferent arteriole to provide negative feedback loops to control water balance

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3
Q

renal response changes in ECF (5):

A
  1. renal sympathetic nerve activity
  2. renin-angiotension II
  3. renin-aldosterone
  4. arginine vasopressin (AVP) aka anti-diuretic hormone (ADH)
  5. atrial natriuretic peptide (ANP)
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4
Q

Renal Sympathetic Nerve Activity:
1. Renal sympathetic nerves

A

a. induces the release of renin –> increases Ang II –> increases TPR, [ADH], and [aldosterone]
b. increase Na reabsorption in the PT –> water reabsorption

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5
Q

Renal Sympathetic Nerve Activity:
2. Renin –> Angiotension II
renin secretion regulated by:

A
  1. sympathetics –> renin release
  2. renal baroreceptors: afferent arteriole sense low pressure –> renin release high pressure inhibits release
  3. macula dense’s osmoreceptors: reduced tubular flow activates osmoreceptors –> renin release
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6
Q

Renal Sympathetic Nerve Activity:
2. Renin –> Angiotension II
effects of angiotensin II

A

a. increase TPR to increase BP
b. stimulate pos. pituitary to release ADH
c. stimulates adrenal cortex to release aldosterone
c. constriction of efferent arteriole –> increase GFR
d. stimulates Na reabsorption in PT by increasing insertion and activity of apical Na-H antiporter

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7
Q

Renal Sympathetic Nerve Activity
2. Renin –> Angiotension II
effects of angiotensin II on brain and glands

A

a. increases the sensation of thirst
b. stimulates posterior pituitary to release vasopressin to increase water reabsorption
c. stimulates aldosterone synthesis and release from adrenal cortex which enhances Na reabsorption

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8
Q

Renal Sympathetic Nerve Activity
3. Renin –> AngII –> Aldosterone
Aldosterone release induced by:

A

a. angiotension II
b. hyperkalemia
c. plasma acidosis

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9
Q

Mechanism of Action of Aldosterone

A

a. primarily acts upon the principal cells of the distal tubule and CD
b. synthesizes apical epithelial Na channels (ENaC)
c. opens apical K+ (loss) both augment Na and water reabsorption

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10
Q

Na enters principal cells via ENaC that can be blocked by the diuretic

A

amiloride

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11
Q

Na reabsorption can be slowed by

A

spironolactone

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12
Q

Renal Sympathetic Nerve Activity
5. Arginine Vasopressin (AVP) aka Anti-diuretic hormone (ADH)
release is stimualted by

A

a. increased osmolarity –> promotes water reabsorption
b. angiotensin II
c. baroreceptors (low pressure)

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13
Q

Antidiuretic hormone MOA

A

promote insertion of aquaporin channels into collecting tubule to drive water reabsorption

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14
Q

Renal Sympathetic Nerve Activity
6. Atrial Natriuretic Peptide (ANP)
Primary effects:

A

PRESSURE OVERLOAD
Hypertension can induce release of ANP from heart
a. promotes Na excretion –> water loss
b. induces systemic vasodilation
c. only released when ECF volume is really expanded
d. inhibits renin and aldosterone secretion

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15
Q

Beneficial Effects of Angiotensin II Blockade

A

a. inhibiting angiotensin II via ACE inhibitors or AT1 receptor blockers) will decrease efferent arteriolar resistance decreasing glomerular capillary pressure

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16
Q

ACE inhibitor or angiotensin II blocker mechanisms

A
  1. reduce efferent arteriolar constriction
  2. lower systemic blood pressure
  3. reduce proteinuria
  4. reduce production of cytokines
    3 and 4 will be on EXAM
17
Q

ACE inhibitors further increase

A

the half-life of bradykinin (vasodilator of afferent arteriole) which promotes the dilation of afferent arterioles and increases GFR and RBF

18
Q

Diabetes (high blood sugar) leads to an increase in a unique

A

Na-Glucose co-transporter (SGLT2) in the proximal tubule
- SGLT2 alters tubuloglomerular feedback leading to
a. dilation of afferent arteriole by NO
b. constriction of efferent
c. increase filtration pressure, Pgc, and GFR
d. hyper-filtration and glomerulosclerosis

19
Q

Diuretics function

A

inhibit Na reabsorption
prevents Cl- reabsorption
prevents osmotic gradient for water reabsorption

20
Q

Osmotic Diuretics MOA and location

A
  1. proximal tubule
    unreabsorbable solutes such as mannitol
    they are used in cases of acute fluid overload
21
Q

Carbonic Anhydrase Inhibition MOA and location

A
  1. proximal tubule
    acetazolamide is inhibitor of CA which slows the Na-H exchanger on the apical membrane
    - reduces H+ excretion resulting in metabolic acidosis
22
Q

Loop Diuretics MOA and location

A
  1. TAL of loop of henle
    Furosemide (Lasix) are used to treat acute pulmonary edema and patients with congestive heart failure
    - they work by blocking Na/K/2Cl co-transporter
23
Q

Thiazide Diuretics MOA and location

A
  1. distal convoluted tubule
    block the Na/Cl co-transporter
    limits Na re-absorption and promotes water excretion
    promotes Ca reabsorption
    there is still net Na and water loss
    lowers BP and treats kidney stones resulting from hypercalciuria
    help treat osteoporosis
24
Q

Amiloride Diuretic MOA and location

A

K+ sparing diuretics
1. collecting duct –> principal cells
- inhibits ENaC which prevents Na reabsorption and leads to water excretion

25
Q

Spironolactone MOA and location

A

K+ sparing diuretics
1. collecting duct –> principal cells
- block aldosterone receptors
promotes Na reabsorption and retention of water at expense of K excretion
inhibition of aldosterone leads to Na and water loss