Body fluid homeostasis Flashcards
Semester 1 year 1
Where are antidiuretic hormones released from?
Posterior pituitary gland
How is vasopressin released?
Sits in vesicles where it waits for signal to be fused with the presynaptic membrane where it’s secreted
Where is the signal that initiates the release of antidiuretic hormones released from?
Neurosecretory neurons
What does ADH do?
-regulates body fluid osmolality
-conserves H2O by reducing urinary losses
How is blood plasma concentration returned to normal using ADH when body fluid osmolality is increased?
-increased blood fluid osmolality
-causes increased plasma conc.
-so increased ADH
-so less water lost in urine
-plasma conc. returned to normal
How is blood plasma concentration returned to normal using ADH when body fluid osmolality is decreased ?
-decreased body fluid osmolality
-causes decreased plasma conc.
-so decreased ADH
-so more water lost in urine
-plasma conc. returned to normal
Where do hypothalamic osmoreceptors sit?
Sub-optic + paraventricular nuclei
How sensitive are hypothalamic osmoreceptors?
-very
-detect changes of +- 3 mosmol/kg H2O
-normal range = 280-300 mosmol/kg H2O
What are hypothalamic osmoreceptors stimulated by and what is their response?
-stimulated by increased osmolality
-release ADH from posterior pituitary
-feeling of thirts
What causes an increased plasma osmolality?
-solute ingestion or H2O deficiency
-stress + drugs (nicotine, ecstasy)
What causes a decreased osmolality plasma?
-excessive fluid ingestion
-alcohol
At normal plasma osmolality, is there ADH circulating?
Yes
Does urine osmolality go to 0?
-no
-we can never not produce urine
-always have to excrete waste products of metabolism
As plasma ADH increases, what happens to urinary osmolality?
It increases
Describe the principal cell H2O model
-ADH binds to V2 receptor, initiating signalling cascade
-activates PKA creating active PKA
-phosphorylates proteins in vesicle membranes
-causes vesicles containing AQP2 H2O channels to fuse with principal cell membrane
-more AQP2 channels in membrane
What protein channels aren’t regulated by ADH?
-AQP3
-AQP4
What does having more AQP2 channels in the apical membrane of principal cells lead to?
-increased H2O reabsorption
-dilution of plasma
-fall in body fluid osmolality
-fast response - around 15 mins
What is the effect of diabetes insipidus?
Create copious quantities of dilute urine
Describe central diabetes insipidus and how it can be treated
-no release of ADH
-treatment - nasal spray desmopressin
Describe nephrogenic diabetes insipidus and how it can be treated
-no response to ADH
-caused by gene mutations in the genes coding for V2 receptors or AQP2 channels
-range of treatments
What is aldosterone?
-classed as a mineralocorticoid
-regulates plasma Na+ content, K+ content + body fluid volume
Where is aldosterone released from?
Cortex of adrenal gland by the layer zona glomerulosa
What is aldosterone released in response to?
-increased plasma K+
-decreased plasma Na+ –> usually maintained by osmoregulation (ADH)
-decreased ECF volume - in conjunction with renin-angiotensin system
What does aldosterone act on?
-late distal tubule
-cortical + medullary collecting duct
What happens as a result of aldosterone?
-increased Na+ reabsorption, causing increased H2O reabsorption
-increased secretion of K+ and H+
How does aldosterone act on principal cells?
-cytosolic mineralocorticoid receptor sits inside principal cell
-aldosterone diffuses across the membrane + binds to receptor
-moves to nucleus, then stimulates RNA transcription + protein synthesis
-makes more proteins involved in Na+ reabsorption + K+, H+ secretion
At what level does aldosterone act at?
Acts at level of nucleus to promote transcription
What is the net effect that aldosterone has on alpha intercalated cells?
-increased Na+ transport so:
-increased plasma Na+ content
-H2O increases, so ECF volume increases
-increased driving force for K+ secretion, so decreased plasma K+
-increased driving force for H+, so decreased plasma H+
What is Pseudohypoaldosteronism?
-loss of response to aldosterone due to mineralocorticoid receptor mutations
-urinary Na+ loss but high aldosterone
What does renin-angiotensin regulate?
-body fluid volume
-plasma Na+ and K+
Where is renin released from?
Juxtaglomerular apparatus (JGA)
Describe the renin-angiotensin cascade
-decreased ECF causes release of renin
-causes conversion of angiotensin to angiotensin I to angiotensin II
-active angiotensin II stimulates release of aldosterone from zona glomerulosa
-causes vasoconstriction at arterioles, increasing blood pressure
What is the net effect of the renin-angiotensin cascade and how is it treated?
-increased plasma Na+ content + ECF volume
-results in increased blood pressure
-ACE1 inhibitors are blood pressure treatments
