Final Exam: Hormonal Regulation of Salt and Water Balance Flashcards
(95 cards)
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
2
Q
What is the major electrolyte in the ECF?
A
Na+
3
Q
What does maintenance of vascular volume depend on maintenance of?
A
Na+ balance
4
Q
What are renal mechanisms of Na+ balance regulated by?
A
- RAAS (renin-angiotensin-aldosterone system)
2. Atrial natriuretic peptide
5
Q
When osmolarity and volume are in conflict, what trumps the other?
A
volume regulation trumps constancy of osmolarity; thanks to ADH
6
Q
What is virtually all renal reabsorption due to?
A
- Passive Na+ reabsorption into tubular cells following conc. gradient at luminal surface
- Active Na+ removal from the tubular cells due to the Na+/K+ ATPase pump at basolaterral surface–> keeps tubular intracellular Na+ low
7
Q
What part of the nephron is impermeable to water?
A
Thick Ascending Limb
8
Q
What three hormones regulate NaCl/ H2O? Where are they from?
A
- ADH (antidiuretic hormone; aka vasopressin) from post. pit.
- RAAS (renin-angiotensin-aldosterone) – from kidney-adrenals
- ANP (atrial natriuretic peptide)–> from the heart
9
Q
What is another name for ADH?
A
vasopressin
10
Q
What does ADH signal the kidneys to do?
A
converse H2O
11
Q
Under what two conditions does ADH signal the kidney to conserve H2O?
A
- Released when plasma osmolarity is increased (over 280 mOsm/L)
- Released when plasma volume is decreased at least 10-15%
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
13
Q
What is a powerful vasoconstrictor targeting the arteriolar smooth muscle? Via what receptors is used?
A
ADH
via V1 receptor
14
Q
What is 10x more powerful at vasoconstricting arteriolar smooth muscle than NE or angiotensin II?
A
ADH
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
16
Q
What does ADH make more permeable to H2O and how?
A
Collecting duct via V2 receptors–> causing insertion of aquaporins
17
Q
What is the most potent osmolyte?
A
NaCl
18
Q
Where are Osmole receptors found?
A
in circumventricular organs (esp. organum vasculosum and subfonical organ) near the 3rd ventricle (outside of BBB)
19
Q
Where do the axons from the circumventricular organs project to?
A
ADH producing cells of hypothalamic supraoptic and paraventricular nuclei
20
Q
What will dehydration cause and therefore what occurs with ADH?
A
increase osmolarity–> stimulates ADH
decrease volume (pressure)–> simulates ADH
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
22
Q
What are two dysfunctional states of ADH?
A
- Diabetes insipidis
2. Syndrome of Inappropriate ADH (SIADH)
23
Q
What two hormones does the posterior pituitary secrete?
A
- ADH aka vasopressin
2. Oxytocin
24
Q
Where are most cell bodies located in the posterior pituitary that release ADH? Oxytocin?
A
ADH–> supraoptic nuclei
Oxytocin–> paraventricular nuclei
25
Where are both ADH and oxytocin synthesized and secreted from?
synthesized--> in hypothalamic neurons
| secreted--> from nerve terminals in posterior pituitary
26
What is the major hormone concerned with regulation of body fluid osmolarity?
ADH aka vasopressin
27
What cells does ADH act on in the kidney? Via what type of receptors?
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
28
What is ADH secreted in response to?
increase in plasma osmolarity
29
What second messenger is used for the V2 receptors that ADH binds to in the late DCT and CD?
cAMp--> causes insertion of aquaporin 2 (water channels) in luminal membranes of principal cells in CD--> concentrating urine
30
What is the second messenger used for the V1 receptors that ADH binds to? What does this cause?
IP3/Ca++
causes contraction of vascular smooth muscle
31
What is the net result of ADH acting on V1 receptors?
- contraction of vascular smooth ms
- constriction of arterioles
- increase total peripheral resistance
32
What type of urine will diabetes insipidis produce?
large amounts of dilute urine
33
What are the two types of Diabetes Insipidus?
1. Central
| 2. Nephrogenic
34
What type of diabetes insipidus is when the posterior pituitary is failing to secrete ADH?
Central
35
What type of diabetes inspidus will cause circulating levels of ADH it be low? What about high?
Low--> Central
High--> Nephrogenic
36
What is Central diabetes insipidus result in?
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+
37
What type of diabetes insipidus is when principal cells of the collecting duct are unresponsive to ADH? What is this a defect in?
Nephrogenic
defect in V2 receptors or G-s protein or adenylyl cyclase
(target is unresponsive)
38
T/F. Diabetes insipidus Central and Nephrogenic will have the same result.
True
39
What can Nephrogenic Diabetes insipidus be treated with?
thiazide diuretics --> which inhibit Na+ reabsorption in early distal tubule
40
What is Thiazide diuretics used to treat? How? (3)
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
What disease is due to ADH being secreted from an autonomous site?
Syndrome of inappropriate ADH (SIADH)
42
What is an example of an area that secretes ADH and causes SIADH?
oat cell carcinoma of the lung
43
What does SIADH cause?
Excess H2O reabsorption--> which will:
- dilute body fluids
- decrease plasma osmolarity
- decrease Na+ conc.
44
How is SIADH treated?
with ADH antagonists
Ex: Demeclocycline
or with H2O restriction
45
What are stimulatory factors for ADH, aka vasopressin?
- increase plasma osmolarity
- decrease ECF
- angtiotensin II
- Pain
- nausea
- hypoglycemia
- nicotine
- opiates
- antineoplastic drugs
46
What are inhibitory factors for ADH, aka vasopressin?
- decrease plasma osmolarity
- ethanol
- alpha-adrenergic agonists
- ANP (atrial natriuretic peptide
47
What does ANP promote? Where is it secreted from?
promotes LOSS of fluid
- more ANP--> inhibits ADH
- less ANP --> stimulates ADH
heart
48
Where is renin synthesized and secreted from?
juxtaglomerular cells in walls of afferent renal arterioles
49
What three things stimulate renin release?
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
What three organs are invovled in the RAAS system? What occurs at each?
1. Kidney--> renin released
2. Liver--> angiotensinogen to angiotensin I via renin
3. Lungs--> angtiotensin I to angiotensin II via ACE
51
Where is angiotensin II made in the lungs? By what enzyme?
in pulmonary endothelium as blood perfuses the pulmonary capillaries
by converting enzyme--> ACE
52
Can angiotensin II be produced in other places locally? (besides just by lungs in RAAS) if so, where?
yes
- blood vessels
- adipose
- brain (fxns as NT)
can also produce angiotensinogen, renin, ACE
53
What may these other locations that produce components of RAAS act locoally as?
as a paracrine to stimulate prostaglandins or act as a local growth factor
(role in Na+ regulation and water balance here in unknown)
54
What is the primary signal for release of aldosterone? What will this stimulate?
Angiotensin II
stimulate glomerulosa cells--> to undergo hypertrophy and hyperplasia
55
Does angiotensin II cause vasoconstriction or vascodilation in the kidney? What will this cause?
Vasoconstriction--> decrease renal blood flow and decreases GFR
56
How does angiotensin II decrease renal blood flow and GFR? What does this cause?
- constriction of efferent arterioles will increase colloid pressure in peritubular caps and increase reabsorption here
- increase NaHCO3 reabsorption
57
What effect does angtiotension II have on the heart?
increases cardiac contractility
58
How does angiotensin II redistribute blood flow?
increases to--> brain, heart, and skeletal muscle
decreases--> to skin and viscera
59
What may angiotensin II act as for cardiac and vascular smooth muscle?
as a growth factor
60
What are the actions of angiotensin II in the CNS?
(as both a hormone and NT)
| - stimulates thirst, appetite for Na+, and secretion of ADH
61
Where are receptors for angtiotension II pressent in the CNS?
in hypothalamic cells--> that project to:
1. Supraoptic Nucleus
2. Paraventicular Nucleus
3. other hypothalamic sites (vasomotor centers)
62
What nuclei in the hypothalamus expresses angiotensin II receptors? What does it release in response to stimulation of angiotensin II?
paraventricular nuclei--> release of ADH
| recall: major source of ADH is from supraoptic nucleus though
63
How is the RAAS system regulated? What is the regulated variable?
negative feedback is the major regulator
is blood volume --> which increases as a result of Na+ retention
64
What does ANP stand for? What does it promote the excretion of in the urine?
Atrial Natriuretic Peptide
Na+
65
What are the three "types/ forms" of ANP?
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
What do ANP and BNP bind to? What does CNP bind to?
What do all three bind to?
ANP and BNP--> NPR-A
CNP--> NPR-B
all three--> NPR-C
67
What do all three types, ANP, BNP, and CNP bind to and what may this function as?
NPR-C
widely distributed and may functions as "clearance receptors" removing them from the blood
68
What is the half life of ANP? What is it for BNP?
ANP--> 3 mins
| BNP--> 20 mins
69
What do both ANP and BNP stimulate formation of?
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
What does ANP prevent?
volume overloading
71
What organs/systems does ANP act on? What is the main goal?
1. Cardiovascular system
2. kidneys
3. adrenal glands
4. CNS
to lower blood volume and decrease BP
72
What effect does ANP have on the CV system?
- vasodilation of vascular smooth muscle
73
What effect does ANP have on the kidneys?
- increase Na+ and H2O excretion by increasing GFR and decreasing Na+ and H2O reabsorption
- decrease renin secretion--> and therefore decrease angiotensin II
74
What effect does ANP have on the hypothalamus?
Decrease:
- ADH secretion
- vasomotor activity
- Na+ appetitie
inhibits thirst
75
What effect does ANP have on the pituitary gland?
- inhibits release of ACTH (decrease adrenal support)
76
What effect does ANP have on the adrenal gland?
- decrease aldosterone secretion
77
What effect does ANP have on the SNS?
- may decrease NE release from SNS and decrease Epi release from adrenal medulla
78
What is the interaction of hormonal regulators of BP and blood volume? What will decrease BP and blood vol? What will increase it?
Decrease:
- ANP
Increase:
- ADH
- Angiotensin II
- Aldosterone
79
What happens to osmolarity during hemorrhage?
no change in osmolarity
80
What is the immediate response to hemorrhage?
massive vasoconstriction mediated by SNS (CNS ischemic response)
81
What is the slower response to hemorrhage?
stimulation of RAAS
stimulation of ADH (secondary)
82
What hormone will hemorrhage inhibit?
ANP
83
What will happen to osmolarity during Dehydration (excessive sweating)?
H2O loss is greater than solute loss--> results in increase in both ECF and ICF osmolarity
84
What is the primary way to correct dehydration? Why?
ADH--> b/c it promotes H2O reabsorption w/o reabsorbing solute (excpetion Urea)
85
What does dehydration inhibit?
ANP
86
T/F. A decrease in volumoe always inhibits ANP.
true
87
What will salt loading promote?
excretion of Na+ in urine
| 10x greater than salt deprived subjects
88
What will salt depletion promote?
minimization of excretion of Na+ in urine
89
Based on a study of both salt loading and salt depletion diets fed over 5 days.
What was nearly identical?
What was different?
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
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.
True
91
What is held almost constant on salt loading and salt depletion?
plasma protein conc.
92
What occurs in Salt Loading?
- ADH?
- renin activity?
- ANP?
- aldostetone?
- plasma protein conc.
- ADH levels increase
- plasma renin activity decreases
- ANP increases
- aldosterone decreases
- urine Na+ increases
- volume expansion (+ ANP_
- plasma protein conc. -- no change
93
What occurs in Salt depletion?
- ADH?
- renin activity?
- ANP?
- aldostetone?
- plasma protein conc.
- decrease ADH levels
- plasma renin activity increases
- ANP decreases
- aldosterone increases
-
- plasma protein conc. -- no change
94
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?
1. high salt intake
| 2. low salt intake
95
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?
1. high salt intake
| 2. low salt intake
