salt and water balance

Question 1

aldosterone site of action

Answer 1

collecting tubule and duct

Question 2

angiotensin 2 site of action

Answer 2

proximal tubule, thick ascending loop of henle/disal tubule, collecting tubule

Question 3

ADH

Answer 3

anti diuretic hormone
water loss r regulated by sodium osmolarity
an increase in extra cellular fluid osmolarity causes osmoreceptor cells to shrink, triggering an action potential causing posterior pituitary to release ADH
ADH goes to kidneys to increase water permeability of the DCT/CT.CDs
increased reabsorption of water
H2O is conserved which Na+ solutes continue to be excreted - dilution of ECF solutes

Question 4

ADH is synthesised in

Answer 4

produced in the supraoptic and paraventricular nuclei in the hypothalamus
stored in the posterior pituitary

Question 5

ADH is released when

Answer 5

release is triggered by increase in plasma osmolarity

stimulates exocytosis of ADH into the blood stream

Question 6

what does ADH do

Answer 6

increased water permeability of DCT/CT.CD
retains water
increases aquaporinb activity

Question 7

aquaporin 2

Answer 7

has two states

• can be endocytose into a vesicle so it is not active
• can be expocytosed and presented to the membrane where it can be open

Question 8

how does ADH increase aquaporinb activity

Answer 8

• binds V2 receptors > cAMP > kinases > translocation of aquaporin 2 to the luminal membrane where it is active
• aquaporin 2 cluster together, form water channels that permit rapid H2O diffusion

Question 9

aquaporin 3 and 4

Answer 9

in the basolateral membrane provide a path for water to rapidly exit the cells - not ADH regulated

Question 10

chronic ADH

Answer 10

alo stimulates aquaporinb 2 transcription

Question 11

decrease in ADH concentration affect on aquaporinb 2

Answer 11

causes aquaporinb 2 to be endocytosed

Question 12

renin-angiotensin-aldosterone system

Answer 12

• decrease in renal perfusion - tubuloglomerular feedback - renin is released which converted angiotensinogen to angiotensin 1
• angiotensin 1 has low activity, ACE activates it to angiotensin 2 - high activity, short half life - acts in the systemic circulation and is degraded before it reaches the pulmonary circulation

Question 13

angiotensin 2 affect on the kidney

Answer 13

• increasing activity of sodium potassium pumps which causes more sodium to be retained
• stimulates release and production of aldosterone

Question 14

aldosterone affect on the kidney

Answer 14

• increase sodium potassium pump activity and therefore sodium retention

Question 15

angiotensin 2

Answer 15

high activity, short half life
activated version of angiotensin 1
acts on the systemic circulation and is deactivated before it reaches the pulmonary circulation

Question 16

renin is secreted by

Answer 16

granular cells of the JGA

Question 17

renin is secreted due to

Answer 17

catalysed by tubuloglomerular feedback
when there is a decrease in the amount of sodium in the distal collecting tubules
triggers the release of renin into the plasma

Question 18

renin causes

Answer 18

turns angiotensin 1 to angiotensin2

Question 19

aldosterone

Answer 19

• secreted by adrenal cortex zona glomerulosa

- secretion is mediated by angiotensin 2 and increased local potassium concentration

Question 20

aldosterone action in kidney

Answer 20

steroid
diffuses across plasma membrane and binds mineralocorticoid receptor and becomes a transcription factor when activated
changes transcription in cells o produce more sodium potassium pump and sodium channels

Question 21

ANP

Answer 21

atrial natriuretic peptide

• decreases Na+ and H2o reabsorption
• antagonist of aldosterone and angiotensin
• produced in response to atrial stretch
• inhibits sodium retention mechanism - slows sodium potassium pumps
• increases GFR

Question 22

ANP affect on GFR

Answer 22

increases

Question 23

ANP affect on sodium potassium pumps

Answer 23

slows

Question 24

ANP secreted in response to

Answer 24

atrial stretch - too much venous blood volume

Question 25

when the atria are stretched

Answer 25

ANP releases - increases GFR - decreases renin and aldosterone - increased sodium and H2O excretion

Question 26

potassium regulation

Answer 26

lethal - must be controlled/sequestered inside cells | - intracellular fluid is high in potassium

Question 27

factor that shift K into cells

Answer 27

- insulin - aldosterone - beta adrenergic stimulation - alkalosis

Question 28

factors that shift K out of cells

Answer 28

- insulin deficiency - diabetes - aldosterone deficiency - Addison's disease - beta adrenergic blockade - acidosis - cell lysis - strenuous exercise - increased extracellular fluid osmolarity

Question 29

insulin and adrenaline on potassium

Answer 29

ECF > ICF

Question 30

cell lysis and muscle damage on potassium

Answer 30

ICF > ECF

Question 31

potassium secretion

Answer 31

balance of secretion and resorption regulated section - principle cells (late DCT/CT) by retaining more sodium, more potassium is lost

Question 32

secretion rate of potassium is determined by

Answer 32

- Na/K ATPase activity - K electrochemical gradient - K permeability minimally resorbed

Question 33

K feedback control

Answer 33

local potassium levels are a trigger for aldosterone release - elevated potassium increases aldosterone to stop potassium from being toxic

Question 34

3 mechanisms of K feedback control

Answer 34

- increase in K stimulates NA K ATPase - increase in K stimulates increase in K gradient to drive diffusion - increase in K stimulates aldosterone secretion

Question 35

drinking threshold is regulated by

Answer 35

sodium | increase in extracellular sodium ECF triggers thirst mechanism

Question 36

thirst stimuli

Answer 36

- hypertonicity - hypothalamic osmoreceptors which inactivated thirst mechanisms - hypovolaemia - hypotension - angiotensin 2 - potent dipsinogen all feed into the hypothalamus

Question 37

osmoreceptors are located in

Answer 37

AV3V region receive information for medullary blood pressure centres project to supraoptic and paraventricular nuclei - ADH synthesis

Question 38

2 primary stimuli for salt appetite

Answer 38

- decrease of ECF sodium - decreases thirst/more hunger for salt - decrease of blood pressure increases thirst and salt appetite

Question 39

region that governs salt appetite

Answer 39

AV3V region