Salt and water handling

Question 1

Renin angiotensin aldosterone system

Answer 1

1. Renin released from kidneys n response to stimuli
2. Converts angiotensinogen to Ang I in liver
3. Ang I converted by ACE to ang II which has effect in body both directly and via aldosterone

Question 2

Angiotensin II

Answer 2

1. Na+ reabsorption in the proximal tubule and lielyi distal sites as well
2. At higher concentration causes vasoconstriction
3. releases aldosterone

Question 3

What is the function of aldosterone

Answer 3

Allows Na+ reabsorption in the DCT/collecting duct in exchange for K+

Question 4

Prostaglandins -formation

Answer 4

arachidonic acid released from phospholipids, is metabolized to PGs by cyclooxgenase

Question 5

Prostaglandin action in the kidney

Answer 5

-main PG is PGI2 (i.e. prostacyclin)

Question 6

PGI2 role

Answer 6

=afferent arteriole vasodilation and natriuress

Question 7

Prostaglandins in healthy

Answer 7

-little or no basal PGI12 syntheiss

Question 8

When do prostaglandin levels rise

Answer 8

-in low ECGV states (CHF or cirrhosis) PGI2 levels rise to maintain renal perfusion in the setting of high AII, SNS activity ect

Question 9

NSAIDS in certain people -safety

Answer 9

NSAIDS will remove the counteregulation…

Question 10

How renal sympathetic nerves regulate kidney function

Answer 10

• increase SNS activity leads to renin secretion

- greater activity of SNS also directly causes increase Na+ /H2O reabsorption

Question 11

Kidney transplant patients - effect SNS

Answer 11

-lack renal innervation (cant attach sympathetic nerves during surgery) and therefore seem to be prone to ECF volume depletion

Question 12

Natriuretic peptides

Answer 12

-atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP)

Question 13

Renal effects of natriuretic peptides

Answer 13

-increase GFR and natriuresis (latter effect similar to the poss)

Question 14

Uroguanylin production

Answer 14

gut natriureti peptide

-produced in intestines in response to salt intake (probably as a prohormone)

Question 15

Uroguanylin effect

Answer 15

• reduces renal sodium reabsorption, helping to compensate for ingestion of dietary sodium
• not a target for pharmacological intervention yet

Question 16

Nitric oxide effect

Answer 16

-appears to have diuretic properties (separate from its vasodilatory powers) and NO deficiency or resistance has been implicated in some models of hypertension

Question 17

Salt reabsorption –> major sites in nephron

Answer 17

• total 27000 mmol Na+ is filtered per day excreting 150 mmol of Na+ in a day
  1. Proximal convolutedd tubule filter 27000 mmol –> takes back 18,00 and 9000 travelling more distally
  2. Loop of henle –> reabsorbs 6000, 3000 goes more distally
  3. In cortical collecting duct 700 reabsorbed, 300 remains
  4. In medullary collecting duct 150 reabsorbed 150 remains

Question 18

Water regulation -purpose

Answer 18

-regulated to maintain a physiological [Na+]
-disturbances of Na+ lead to change in ADH secretion
-loss of water = increase Na+ concentration = increase osmolarity leading to cell shrinkage in hypothalamus = increase release of arginine vasopressin (ADH) by posterior pituitary
+ increase thirst (same osmotic stimulus in hypothalamus leads to increased thirst)

Question 19

Effect loss pituitary function

Answer 19

-can lead to loss of adh = central diabetes insipidus –> does not usually impair thirst so can still survive?

Question 20

ADH receptors

Answer 20

2 main vasopressin receptors
V1
V2
(V3)

Question 21

V1 receptor

Answer 21

• located in arterioles, glomerular mesangila cells, and the brain
• mediates vasoconstriction

Question 22

V2 receptor

Answer 22

-located on the blood side…

Question 23

ADH and V1 receptor activation

Answer 23

physiological adh nnot sufficient to cause activation of V1 receptor

Question 24

Non osmotic stimuli of ADH

Answer 24

1. Volume depletion
2. Nausea/vomiting
3. Pain
4. Medications (narcotics, chlorpropamide, carbamazepine)
5. Exercise

Question 25

Half life of endogenous vasopressin

Answer 25

t1/2 of minutes

Question 26

MOA of vasopressin drug

Answer 26

-a selective V1 agonist which can be used in the treatment of shok in the ICU setting

Question 27

DDVP

Answer 27

??

Question 28

What determines the extracellular fluid volume

Answer 28

The serum sodium content (number of Na+ particles)

Question 29

What determines the serum sodium concentration

Answer 29

Determines the intracellular fluid volume (not under direct physiological control due to water permeability of cell mebranes) -no hormones involved in this (automatic)

Question 30

What does serum [Na+] reflect

Answer 30

- the ratio of Na+ to water | - it does not correlate wtih ECFV (volume status) or body sodium content

Question 31

What do alteration in Na+ concentration reflect

Answer 31

- imbalances in the ratio of salt to water | - almost always this is because of disturbance in water content

Question 32

Main intracellular ion vs. extracelluar

Answer 32

Na+ main extracellular, K+ main intracellular

Question 33

What do change in body salt content result in

Answer 33

-corresponding change in body wter content such that ECF volume changes but sodium concentration...

Question 34

MOA cerebral edema/coning

Answer 34

1) Loss Na+ (hyponatremia) --> decrease Na+ content in same volume of fluid = lower Na+ concentration 2) Water therefore flows into the cells to reach a new euiqlibrium (low extracellular osmolality compared with the intracellular space) 3) Water flows into cells to reach new equilibrium 4) Water expands in cells --> edema (conning why??)

Question 35

CHF

Answer 35

1) Reduced CO 2) Decreased presure loading of arterial sensors =decreased effective circulating volume 3) Initiates several processes leading to Na+ retention 4) If the extracellular fluid becomes salty other signals act to retain water as well

Question 36

Effect Na+ a) increased b) decreased

Answer 36

a) edema | b) hypovolemia or shock

Question 37

Effect H2O a) increased b) decreased

Answer 37

a) cerebral edema | b) osmotic demylination

Question 38

How low sodium content leads to low Na+ concentration via ADH

Answer 38

1) Decreased Na+ | 2) Decreased sodium concentration (via ADH induced H2O retention)

Question 39

What is being sensed a) osmoregulation b) volume regulation

Answer 39

1) plasma osmolarity | 2) volume regulation

Question 40

Sensors a) osmoregulation b) volume regulation

Answer 40

X

Question 41

X

Answer 41

X

Question 42

X

Answer 42

X

Question 43

How to change the concentration of urine

Answer 43

X

Question 44

x

Answer 44

1. Prox tubule = lots of isotonic reabsorption 2. Descending lumb = concentrating segment = water reabsorbed but salt isnt 3. Ascending limb = diluting segment = solutes reabsorbed 4. Distal tubule = some additional salt/H2O reabsorbtion but in general urine remains diluted (relative to the blood): 5. Collecting duct: if ADH acting, water reabsorbed down its gradient, otherwise urine remains dilute

Question 45

Diluting the urine - requirements

Answer 45

TAL must be functioning in order to create.

Question 46

Concentrating the urine MOA

Answer 46

Water must be removed to leave behind a concentrated urine