Body Fluid Homeostasis

Question 1

vasopressin

Answer 1

antidiuretic hormone, ADH
released from posterior pituitary gland
made in cell body of neurons, travels down axon and stored in vesicles
when ap generated in neurosecretory neurons, ap caused fusion of vesicles containing vasopressin to membrane and it be released
diffuses into circulation in venous blood supply
target organ = kidney

Question 2

vasopressin function

Answer 2

regulates body fluid osmolality (con of body fluid), conserves H2O
inc body fluid = inc vasopressin = conserves water, more water in plasma, conc plasma dec in osmolality
dec osmolality = inc vasopressin, excrete higher urine flow rate, plasma becomes more conc

Question 3

hypothalmic receptors

Answer 3

sensitive to conc changes in plasma
detect change of +/- 3 mosmol/kg H2O
supraoptic and periventricular nuclei regions of hypothalamus
stimulation of osmoreceptors - leads to action potnetial (inc osmolality)
a) release vasopressin from posterior pituitary
b) feeling of thirst

Question 4

regulation of release

increase

Answer 4

inc release = inc osmol of plasma = inc water retention
solute ingestion or H2O deficiency
stress and drugs - nictoine and ecstasy

Question 5

regulation of release

decrease

Answer 5

dec release = dec osmol in plasma
excessive fluid ingestion
alcohol - inhibits release of vasopressin, excrete more water - dehydration

Question 6

principle cell H2O model

Answer 6

vasopressin in peritubular capillaries
diffuses into interstitial fluid, binds to vasopressin receptor (V2)
activation of V2 activates signalling molecule - protein kinase A = mediates phosphorylation which leads to insertion of vesicles under apical mem and fuse
AQP2 in vesicle mem = now in apical membrane as vesicles fuse
inc vaso = inc AQP2 = inc water reab
when vaso dec, AQP channels are pulled out of membrane

Question 7

net effect of vasopressin

Answer 7

increased vaso = inc H2O reab = dec body fluid osmolality

Question 8

diabetes insipidus

Answer 8

problems with AQP2, vasopressin and H2O reab
copious quantities of dilute urine - 23L/day = dehydration
central diabetes = no release of vaso - treatment = nasal spray DDAVP = synthetic vasopressin
nephrogenic diabetes = defect at level of kidney = no response to vaso, defect in V2 receptor = cant bind vaso or activate cAMP and protein kinase A or defect in AQP2 channel - range of treatments

Question 9

aldosterone

Answer 9

released from cortex of adrenal gland - zona glomerulosa layer
classed as mineralocorticoid, regulates plasma Na, K and body fluid vol
released in response to: inc plasma K, dec plasma Na, dec ECF vol
acts on late distal tubule and collecting duct on both principle and IC cells
causes - inc reab Na so inc reab H2O, inc secretion K and H

Question 10

principle cell genomic action

Answer 10

aldosterone = mem soluble, can pass through bilayer, diffuses into cell
mineralocortidcoid receptor inside cell is bound by aldosterone
this complex moves to nucleus, stimulates RNA transcription and protein synthesis = genomic action
e.g. promotes production of ENaC, ROMK and NaH exchanger
slow action

Question 11

alpha IC cell genomic action

Answer 11

inc protein synthesis for ATP/H pump to allow cell to secrete more H into tubular fluid into urine

Question 12

net effect in principle and IC cell

Answer 12

inc plasma Na so inc ECF vol, dec plasma K, dec plasma H

co-ordinate regulation with renin-angiotensin system

Question 13

liddles syndrome

Answer 13

hypertension
high Na reab at collecting ducts eventhough aldosterone levels are low, too many Na in principle cell so reab too much Na - water follows = hypertension

Question 14

pseudohypoaldosteronism

Answer 14

salt loss, water loss, hypotension but high aldosterone

loss of response to aldo, problem with mineralo receptor

Question 15

renin-angiotensin

Answer 15

regulates body fluid, plasma Na, K

renin - released from juxtaglomerular apparatus (JGA)

Question 16

JGA

Answer 16

macula densa cell - for conc of tubular fluid and flow rate, release chemicals that control delivery of plasma to capillary bed
sumpathetic nerves control release of renin
granular cells - contain renin, when activated they release renin into plasma

Question 17

renin-angio cascade

Answer 17

dec ECF vol ——> stimulates renin release by JGA ——> renin goes into circulation and catalyses angiotensinogen (made by liver) –> angiotensin 1 ——-> under influence of angiotensin converting enzymes (ACE) found in capillaries angio1 is converted into angiotensin II (active) - mostile produced in lungs

Question 18

angiotensin II

Answer 18

acts at zona glomerulosa level - releases aldosterone
arterioles: vasoconstriction, inc blood pressure
net effect = inc plasma Na and ECF vol, inc blood pressure
people with high blood pressure have ACE inhibitors to prevent excess production of angio II

Question 19

integration - volume vs osmolality

Answer 19

ingest salt: inc plasma Na and H2O moves out of interstital fluid
= inc ECF vol and inc osmol in plasma

Question 20

increased ECF vol

Answer 20

dec aldosterone
inc loss Na
inc loss H2O
dec ECF vol

Question 21

increased osmolality of plasma

Answer 21

inc vasopressin
inc reab H2)
dec osmolality
but inc ECFV
so vasopressin system is reset in terms of sensitivity of system to osmol

Question 22

dec vs inc plasma vasopressin

Answer 22

dec = volume expansion so bigger change in osmol needed to release same amount of vaso
inc = volume depletion leads to lost fluid e.g. haemorrage