body fluid homeostasis Flashcards
what’s ADH
-antidiuretic hormone
-regulates blood fluidity
-conserves H2O by reducing urinary loss
-if there is an increase in body fluid osmolality then there will be an increase of ADH vice versa
what are hypothalamic osmoreceptors
-proteins which sit in the membrane of neurone secretory membranes
-supra-optic and paraventricular nuclei
-very sensitive so they detect + or - 3 mosmol/kg H2O
-normal range is 280-300 mosmol/kg H2O
-stimulated by an increase in osmolality
how is ADH regulated and released
-increase in osmolality plasma stimulates release of ADH, solute ingestion or H2O deficiency, stress and drugs- nicotine and ecstasy
-decrease in osmolality in the plasma leads to excessive fluid ingestion and may be caused by drugs and alcohol
-alcohol inhibits release of ADH therefore less reabsorption of water by the kidney, more excretion of water in the urine
-ecstasy stimulates the release of ADH even when non is needed, ADH therefore goes to kidneys and promotes water reabsorption and an increase in water drinking which causes a build up of water in the brain leading to adema
ADH and urine osmolality
-as plasma ADH increases urinary osmolality increases
-never goes to 0 as we never dont produce any urine due to waste products of metabolism which. need to be excreted
how does ADH work on the principle cells
-V2 receptor (vasopressin) on BM of principle cells
-ADH in peritubular capillaries diffuse out into interstitial fluid and binds to V2 receptor and initiates signalling cascade which activate protein kinase A (PKA) which phosphorylates proteins
-in principle cell PKA phosphorylates proteins found in vesicles found underneath AM
-in membrane of these vesicles aquaporin 2 channel are present
-due to phosphorylation, there is an increase in AQP2 channels, the more water channels= more water reabsorbed in principle
-with high ADH there is lots of AQP2, meaning lots of water reabsorption so plasma is diluted
-AQP3 and 4 not regulated by ADH- constitutenly active- lots of them and always open
-this is called membrane shuttling hypothesis
what’s the net effect of this shuttling hypothesis
-more AQP2 channels in the AM
-increase in reabsorption of water
-dilution of plasma
-fall in body fluid osmolality
-fast response
what’s diabetes insipidus
-copious quantities dilute urine - 23l/day
-central DI- problems with posterior pituitary gland therefore can’t relate ADH, treatment is nasal spray desmopressin
-nephrogenic DI- ADH released no responded to- defect in the V2 receptor, AQP2 channels, range of treatments
what’s aldosterone
-its released from the cortex of the adrenal gland from zona glomerulosa mineralocorticoid , regulates plasma Na+, K+ and body fluid volume
-released in response to:
=increased plasma K+ =0.1mM
=decrease in plasma Na+ - minor concentration maintained by osmoregulation ADH
=decrease in ECF volume- via renin-angiotensin
where does aldosterone act
-in late distal tubule and cortical and medullary collecting duct
-causes: increase in reabsorption of Na+, therefore reabsorption of H2O, and secret of K+ and H+
principle cells and their genomic action
-stimulates production of new protein
1) cytosolic mineralocorticoid receptor
2)moves to the nucleus
3)RNA transcription and protein synthesis
4)Na+ reabsorption, K+ selection and H+ secretion
-NaK ATPase channel on BM, as well as a K+ channel
-Na+ channel on AM, K+ channel on AM (leaving), NaH channel so Na+H+ channel where Na+ moves in and H+ out
alpha intercalated cells and aldosterone
-aldosterone diffuses into the cell
-aldosterone moves the the nucleus
-stimulates transcription and protein synthesis
-enhances H+ secretion as a consequence
net effect of aldosterone in alpha intercalated cells
-increased Na+ transport :
=increases plasma Na+ content
=H2O follows and there is an increase in ECF volume
=increases driving force for K+ secretion which decreases plasma K+
=increases driving force for H+ secretion which decreases plasma K+
what does renin-angiotensin regulate
- body fluid volume and plasma Na+ and K+
-renin- released from juxtaglomerular apparatus
what’s JGA
-juxtaglomerular appartus
-contains macula densa cells- specialised ability to release chemicals that impact granular cells which contain the renin
what’s the renin- angiotensin cascade
-if there is a fall in the ECF volume, this leads to stimulation of release of renin in JGA through signalling from macula dense cell
-renin catalyses in blood vessel of conversion of angiotensinogen to angiotensin I
-angiotensin I is then converted to angiotensin II which angiotensin converting enzyme 1- takes place in capillaries
-most made in lungs due to high density of capillaries in lungs
-AE2 is active component- then goes to adrenal gland to stimulate release of aldosterone
