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Endocrinology -- Freedman > Final Exam: Hormonal Regulation of Salt and Water Balance > Flashcards

Final Exam: Hormonal Regulation of Salt and Water Balance Flashcards

1
Q

What is osmolarity of the ECF adjusted by based on the monitoring we have for it?

A

water excretion by kidney in response to ADH

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2
Q

What is the major electrolyte in the ECF?

A

Na+

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3
Q

What does maintenance of vascular volume depend on maintenance of?

A

Na+ balance

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4
Q

What are renal mechanisms of Na+ balance regulated by?

A
  1. RAAS (renin-angiotensin-aldosterone system)

2. Atrial natriuretic peptide

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5
Q

When osmolarity and volume are in conflict, what trumps the other?

A

volume regulation trumps constancy of osmolarity; thanks to ADH

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6
Q

What is virtually all renal reabsorption due to?

A
  1. Passive Na+ reabsorption into tubular cells following conc. gradient at luminal surface
  2. Active Na+ removal from the tubular cells due to the Na+/K+ ATPase pump at basolaterral surface–> keeps tubular intracellular Na+ low
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7
Q

What part of the nephron is impermeable to water?

A

Thick Ascending Limb

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8
Q

What three hormones regulate NaCl/ H2O? Where are they from?

A
  1. ADH (antidiuretic hormone; aka vasopressin) from post. pit.
  2. RAAS (renin-angiotensin-aldosterone) – from kidney-adrenals
  3. ANP (atrial natriuretic peptide)–> from the heart
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9
Q

What is another name for ADH?

A

vasopressin

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10
Q

What does ADH signal the kidneys to do?

A

converse H2O

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11
Q

Under what two conditions does ADH signal the kidney to conserve H2O?

A
  1. Released when plasma osmolarity is increased (over 280 mOsm/L)
  2. Released when plasma volume is decreased at least 10-15%
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12
Q

What are blood volume changes sensed by? Which are thought to be more important?

A

both high and low pressure receptors

low thought to be more important in detection of changes in blood volume

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13
Q

What is a powerful vasoconstrictor targeting the arteriolar smooth muscle? Via what receptors is used?

A

ADH

via V1 receptor

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14
Q

What is 10x more powerful at vasoconstricting arteriolar smooth muscle than NE or angiotensin II?

A

ADH

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15
Q

What will ADH acting on V1 receptors cause? What will it cause acting on V2 receptors?

A

V1–> vasocontriction of arterial smooth muscle

V2–> causes insertion of aquaporins–> making collecting duct permeable to H2O

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16
Q

What does ADH make more permeable to H2O and how?

A

Collecting duct via V2 receptors–> causing insertion of aquaporins

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17
Q

What is the most potent osmolyte?

A

NaCl

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18
Q

Where are Osmole receptors found?

A

in circumventricular organs (esp. organum vasculosum and subfonical organ) near the 3rd ventricle (outside of BBB)

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19
Q

Where do the axons from the circumventricular organs project to?

A

ADH producing cells of hypothalamic supraoptic and paraventricular nuclei

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20
Q

What will dehydration cause and therefore what occurs with ADH?

A

increase osmolarity–> stimulates ADH

decrease volume (pressure)–> simulates ADH

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21
Q

What happens if we have a decrease in osmolarity but an increase in volume?
What if it is a small increase in vol? What if it is a large increase in vol?

A

osmolarity is kept constant is volume depletion is small

BUT, if volume loss is large, osmolarity is sacrificed to maintain integrity of circulation

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22
Q

What are two dysfunctional states of ADH?

A
  1. Diabetes insipidis

2. Syndrome of Inappropriate ADH (SIADH)

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23
Q

What two hormones does the posterior pituitary secrete?

A
  1. ADH aka vasopressin

2. Oxytocin

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24
Q

Where are most cell bodies located in the posterior pituitary that release ADH? Oxytocin?

A

ADH–> supraoptic nuclei

Oxytocin–> paraventricular nuclei

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25
Q

Where are both ADH and oxytocin synthesized and secreted from?

A

synthesized–> in hypothalamic neurons

secreted–> from nerve terminals in posterior pituitary

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26
Q

What is the major hormone concerned with regulation of body fluid osmolarity?

A

ADH aka vasopressin

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27
Q

What cells does ADH act on in the kidney? Via what type of receptors?

A

principal cells in late Distal Convoluted Tubule and Collecting Duct–> to increase H2O re-absorption–> to decrease body fluid osmolarity back to normal

via V2 receptors

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28
Q

What is ADH secreted in response to?

A

increase in plasma osmolarity

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29
Q

What second messenger is used for the V2 receptors that ADH binds to in the late DCT and CD?

A

cAMp–> causes insertion of aquaporin 2 (water channels) in luminal membranes of principal cells in CD–> concentrating urine

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30
Q

What is the second messenger used for the V1 receptors that ADH binds to? What does this cause?

A

IP3/Ca++

causes contraction of vascular smooth muscle

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31
Q

What is the net result of ADH acting on V1 receptors?

A
  • contraction of vascular smooth ms
  • constriction of arterioles
  • increase total peripheral resistance
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32
Q

What type of urine will diabetes insipidis produce?

A

large amounts of dilute urine

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33
Q

What are the two types of Diabetes Insipidus?

A
  1. Central

2. Nephrogenic

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34
Q

What type of diabetes insipidus is when the posterior pituitary is failing to secrete ADH?

A

Central

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35
Q

What type of diabetes inspidus will cause circulating levels of ADH it be low? What about high?

A

Low–> Central

High–> Nephrogenic

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36
Q

What is Central diabetes insipidus result in?

A

since post. pit is failing to secrete ADH–> circulating levels of ADH are LOW–> therefore CD stay impermeable to H2O–> produces large amounts of dilute urine–> and that will incrase plasma osmolarity and Na+

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37
Q

What type of diabetes insipidus is when principal cells of the collecting duct are unresponsive to ADH? What is this a defect in?

A

Nephrogenic

defect in V2 receptors or G-s protein or adenylyl cyclase

(target is unresponsive)

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38
Q

T/F. Diabetes insipidus Central and Nephrogenic will have the same result.

A

True

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39
Q

What can Nephrogenic Diabetes insipidus be treated with?

A

thiazide diuretics –> which inhibit Na+ reabsorption in early distal tubule

40
Q

What is Thiazide diuretics used to treat? How? (3)

A

Nephrogenic diabetes insipidus

  • inhibits Na+ reabsorption in early Distal Tubule–> this prevents dilution of urine
  • decreases GFR (so less H2O is filtered, therefore less secreted)
  • by increasing Na+ excretion–> can cause secondary ECF volume contraction–> in response we have reabsorption of solutes and H2O increase and less H2O excreted
41
Q

What disease is due to ADH being secreted from an autonomous site?

A

Syndrome of inappropriate ADH (SIADH)

42
Q

What is an example of an area that secretes ADH and causes SIADH?

A

oat cell carcinoma of the lung

43
Q

What does SIADH cause?

A

Excess H2O reabsorption–> which will:

  • dilute body fluids
  • decrease plasma osmolarity
  • decrease Na+ conc.
44
Q

How is SIADH treated?

A

with ADH antagonists

Ex: Demeclocycline

or with H2O restriction

45
Q

What are stimulatory factors for ADH, aka vasopressin?

A
  • increase plasma osmolarity
  • decrease ECF
  • angtiotensin II
  • Pain
  • nausea
  • hypoglycemia
  • nicotine
  • opiates
  • antineoplastic drugs
46
Q

What are inhibitory factors for ADH, aka vasopressin?

A
  • decrease plasma osmolarity
  • ethanol
  • alpha-adrenergic agonists
  • ANP (atrial natriuretic peptide
47
Q

What does ANP promote? Where is it secreted from?

A

promotes LOSS of fluid

  • more ANP–> inhibits ADH
  • less ANP –> stimulates ADH

heart

48
Q

Where is renin synthesized and secreted from?

A

juxtaglomerular cells in walls of afferent renal arterioles

49
Q

What three things stimulate renin release?

A
  1. SNS activation assoc. with a decrease in BP sensed by baroreceptors (carotid and aortic)
  2. decrease tension on afferent arterioles in glomerulus
  3. decrease pressure in glomerulus –> which decreases rate of NaCl delivery to macula densa
50
Q

What three organs are invovled in the RAAS system? What occurs at each?

A
  1. Kidney–> renin released
  2. Liver–> angiotensinogen to angiotensin I via renin
  3. Lungs–> angtiotensin I to angiotensin II via ACE
51
Q

Where is angiotensin II made in the lungs? By what enzyme?

A

in pulmonary endothelium as blood perfuses the pulmonary capillaries

by converting enzyme–> ACE

52
Q

Can angiotensin II be produced in other places locally? (besides just by lungs in RAAS) if so, where?

A

yes

  • blood vessels
  • adipose
  • brain (fxns as NT)

can also produce angiotensinogen, renin, ACE

53
Q

What may these other locations that produce components of RAAS act locoally as?

A

as a paracrine to stimulate prostaglandins or act as a local growth factor

(role in Na+ regulation and water balance here in unknown)

54
Q

What is the primary signal for release of aldosterone? What will this stimulate?

A

Angiotensin II

stimulate glomerulosa cells–> to undergo hypertrophy and hyperplasia

55
Q

Does angiotensin II cause vasoconstriction or vascodilation in the kidney? What will this cause?

A

Vasoconstriction–> decrease renal blood flow and decreases GFR

56
Q

How does angiotensin II decrease renal blood flow and GFR? What does this cause?

A
  • constriction of efferent arterioles will increase colloid pressure in peritubular caps and increase reabsorption here
  • increase NaHCO3 reabsorption
57
Q

What effect does angtiotension II have on the heart?

A

increases cardiac contractility

58
Q

How does angiotensin II redistribute blood flow?

A

increases to–> brain, heart, and skeletal muscle

decreases–> to skin and viscera

59
Q

What may angiotensin II act as for cardiac and vascular smooth muscle?

A

as a growth factor

60
Q

What are the actions of angiotensin II in the CNS?

A

(as both a hormone and NT)

- stimulates thirst, appetite for Na+, and secretion of ADH

61
Q

Where are receptors for angtiotension II pressent in the CNS?

A

in hypothalamic cells–> that project to:

  1. Supraoptic Nucleus
  2. Paraventicular Nucleus
  3. other hypothalamic sites (vasomotor centers)
62
Q

What nuclei in the hypothalamus expresses angiotensin II receptors? What does it release in response to stimulation of angiotensin II?

A

paraventricular nuclei–> release of ADH

recall: major source of ADH is from supraoptic nucleus though

63
Q

How is the RAAS system regulated? What is the regulated variable?

A

negative feedback is the major regulator

is blood volume –> which increases as a result of Na+ retention

64
Q

What does ANP stand for? What does it promote the excretion of in the urine?

A

Atrial Natriuretic Peptide

Na+

65
Q

What are the three “types/ forms” of ANP?

A
  1. “ANP”–synthesized and secreted from atrial myocytes (in response to increase atrial pressure/stretch)
  2. “BNP”–synthesized and secreted by atrial and ventricles and has been isolated from brain (brain natriuretic peptide)
  3. “CNP”–> found in CNS and endothelial cells is similar
66
Q

What do ANP and BNP bind to? What does CNP bind to?

What do all three bind to?

A

ANP and BNP–> NPR-A

CNP–> NPR-B

all three–> NPR-C

67
Q

What do all three types, ANP, BNP, and CNP bind to and what may this function as?

A

NPR-C

widely distributed and may functions as “clearance receptors” removing them from the blood

68
Q

What is the half life of ANP? What is it for BNP?

A

ANP–> 3 mins

BNP–> 20 mins

69
Q

What do both ANP and BNP stimulate formation of?

A

cyclic GMP–> which modify celular functiosn via one of 3 mechanisms

  1. phosphorylation of regulatory proteins
  2. cyclic nucleotide phosphodiesterases
  3. direct ion channel regulation
70
Q

What does ANP prevent?

A

volume overloading

71
Q

What organs/systems does ANP act on? What is the main goal?

A
  1. Cardiovascular system
  2. kidneys
  3. adrenal glands
  4. CNS

to lower blood volume and decrease BP

72
Q

What effect does ANP have on the CV system?

A
  • vasodilation of vascular smooth muscle
73
Q

What effect does ANP have on the kidneys?

A
  • increase Na+ and H2O excretion by increasing GFR and decreasing Na+ and H2O reabsorption
  • decrease renin secretion–> and therefore decrease angiotensin II
74
Q

What effect does ANP have on the hypothalamus?

A

Decrease:

  • ADH secretion
  • vasomotor activity
  • Na+ appetitie

inhibits thirst

75
Q

What effect does ANP have on the pituitary gland?

A
  • inhibits release of ACTH (decrease adrenal support)
76
Q

What effect does ANP have on the adrenal gland?

A
  • decrease aldosterone secretion
77
Q

What effect does ANP have on the SNS?

A
  • may decrease NE release from SNS and decrease Epi release from adrenal medulla
78
Q

What is the interaction of hormonal regulators of BP and blood volume? What will decrease BP and blood vol? What will increase it?

A

Decrease:
- ANP

Increase:

  • ADH
  • Angiotensin II
  • Aldosterone
79
Q

What happens to osmolarity during hemorrhage?

A

no change in osmolarity

80
Q

What is the immediate response to hemorrhage?

A

massive vasoconstriction mediated by SNS (CNS ischemic response)

81
Q

What is the slower response to hemorrhage?

A

stimulation of RAAS

stimulation of ADH (secondary)

82
Q

What hormone will hemorrhage inhibit?

A

ANP

83
Q

What will happen to osmolarity during Dehydration (excessive sweating)?

A

H2O loss is greater than solute loss–> results in increase in both ECF and ICF osmolarity

84
Q

What is the primary way to correct dehydration? Why?

A

ADH–> b/c it promotes H2O reabsorption w/o reabsorbing solute (excpetion Urea)

85
Q

What does dehydration inhibit?

A

ANP

86
Q

T/F. A decrease in volumoe always inhibits ANP.

A

true

87
Q

What will salt loading promote?

A

excretion of Na+ in urine

10x greater than salt deprived subjects

88
Q

What will salt depletion promote?

A

minimization of excretion of Na+ in urine

89
Q

Based on a study of both salt loading and salt depletion diets fed over 5 days.

What was nearly identical?
What was different?

A

identical–> Na+ conc. and systolic BP
–> osmolarity and Na+ conc. of body fluids were held almost constant*

Different:
High salt diet–> increase in ECF vol
Low salt diet–> decrease in ECF

90
Q

T/F. For high salt or low salt diets, osmolarity and Na+ conc. of body fluids were held almost constant even though there was an increase in ECF for high salt diet and a decrease in ECF for low salt diets.

A

True

91
Q

What is held almost constant on salt loading and salt depletion?

A

plasma protein conc.

92
Q

What occurs in Salt Loading?

  • ADH?
  • renin activity?
  • ANP?
  • aldostetone?
  • plasma protein conc.
A
  • ADH levels increase
  • plasma renin activity decreases
  • ANP increases
  • aldosterone decreases
  • urine Na+ increases
  • volume expansion (+ ANP_
  • plasma protein conc. – no change
93
Q

What occurs in Salt depletion?

  • ADH?
  • renin activity?
  • ANP?
  • aldostetone?
  • plasma protein conc.
A
  • decrease ADH levels
  • plasma renin activity increases
  • ANP decreases
  • ## aldosterone increases
  • plasma protein conc. – no change
94
Q

A study: human volunteers consumed one of three diets: high salt, normal salt, low salt, for 5 days.

  1. What group showed an inhibition of renin and aldosterone?
  2. What group showed an elevation in renin and aldosterone?
A
  1. high salt intake

2. low salt intake

95
Q

A study: human volunteers consumed one of three diets: high salt, normal salt, low salt, for 5 days.

  1. What group showed an increase in ADH?
  2. What group showed a decrease in ADH?
A
  1. high salt intake

2. low salt intake

Endocrinology -- Freedman (14 decks)

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