regulation of osmolarity Flashcards
what is water regulation controlled by
ADH (vasopressin)
where is ADH synthesised
in the supraoptic an dparaventricular nuclei of the hypothalamus in brain
where is ADH released from
posterior pituitary
what effects ADH secretion
primary control is plasma osmolarity
also ECF volume
what happens to ADH secretion when plasma osmolarity increases
increase release of ADH
what are changes in neuronal discharge mediated by
osmoreceptors
osmoreceptors: increased osmolairy
H2O leaves cell
cell shrinks - stretch sensitive ion channel activated
inc neural dischare
inc ADH secretion
osmoreceptors: decreased osmolarity
H2O enters cell
cell swells
decrease neural discharge
dec ADH secretion
normal plasma osmolality
280-290mOsm/kg H2O
regulated very preciscely
why ‘effecitive’ osmolarity
an increase in osmolarity that does not cause an increase in tonicity is ineffective in causing increase in ADH
solutes that can penetrate membranes move together with water and don’t produce any ‘osmotic drag’ or tonictiy
what does amount of urine produced depend on
[ADH]
amount of solute to be excreted
ingestion of hypertonic solutions (e.g. seawater)
increase solute load to be excreted –> inc urine flow –> dehydration as more water required to excrete solute load than was ingested with it
what does ADH act on to control permeability collecting duct
H2O channels in luminal membrane (aquaporins)
if ADH is present
water is able to leave collecting duct
this means cortical CD becomes equilibrated with that of cortical interstitium ie 300
with maximal ADH
produce small volume of highly concentrated urine
- relatively less of filtered water than solute
- compensate for water deficit
absence of ADH
collecting duct impermeable to water
large volume of dilute urine is excreted
-compensate for water excess
role of urea
in presence of ADH, water moves out CF and greatly concentrates urea. CD is relatively permable to urea, esp at medullary tips
as urea approaches medullary tips it moves out down conc gradien into interstitium where it acts to reinforce the interstition gradient in the region of asc loops of henle
urea recycling during maximum anti-diuresis
in anti-diuresis with high levels ADH, urea is retained in order to save water and reinforce medullary gradient at ascending limb LoH
ureaemia occurs
what would happen iif urea wasnt reabsorbed
it would remain in tubule and exert osmotic effects to hold water in tubule and reduce potential for rehydration
how does ECF volume effect ADH secretion
inc ECF volume –> less ADH
dec ECF volume –? more ADH
where are low P receptors located
L and R atria
great veins
where are high P receptors located
carotid and aortic arch baroreceptors
relationship between ADH secertion and discharge of stretch P receptors
inverse relationship between rate of ADH secretion and rate of discharge of stretch receptor afferents in the low and high P areas of circulation
other stimuli affecting ADH: more ADH
pain emotion stress excercise nicotine morphine
other stimuli affecting ADH: less ADH
alcohol
diabetes insipidu s
ADH deciciency
