Body Fluid Homeostasis Flashcards
Hormone: Vasopressin (Anti-diuretic hormone ADH)
- Synthesis and storage
- Originates in neurosecretory neurons
- Synthesised in hypothalamus
- Moves to pituitary stalk
- To posterior pituitary (stored in presynaptic vesicles)
- AP->fusion of vesicles->ADH release->enters venous system
Hormone: Vasopressin (Anti-diuretic hormone ADH)
- Function
- Regulates body fluid osmolality (conc of plasma)
- Conserves H2O
- which also regulates conc of Na
- increase body fluid osmolality = increase vasopressin (conserves water)
- decrease body fluid osmolality = decrease vasopressin (suppressed)
Hypothalamic Osmoreceptors
- Detect change of +/- 3mosmol/kg H2O
- V. sensitive
- Located in supra-optic and paraventricular nuclei in hypothalamus
- Stimulation (increased osmolality) causes:
- release of vasopressin from posterior pituitary
- feeling of thirst
Reasons for increased release of vasopressin
Increased plasma osmolality
- Solute ingestion/ H2O deficiency
- Stress and drugs
- nicotine
- 3,4-methylenedioxymethamphetamine (ecstasy)
- water retention - oedema
Reasons for decreased release of vasopressin
Dcreased plasma osmolality
- Excessive fluid ingestion
- Drugs
- alcohol
Principal Cell Model of V2 (vasopressin) receptor
Shuttling Hypothesis
- Vasopressin (V2) receptor on basolateral membrane
- Activates PKA
- catalyses phosphorylation of other proteins
- Allows insertion of vesicles
- AQP2 H2O channels into apical membrane
- reabs more water
- Net effect
- Reabs H2O
- Fall in body fluid osmolality
- 23L/day (max urine) (vasopressin=0)
Diabetes Insipidus
- Sign
- 2 types
- Reason
- Treatment
- Copious quantities of dilute urine ~23L/day
- Central DI (defect in CNS)
- No release of vasopressin
- Nasal spray DDAVP
- Stimulates AQP2
- Nephrogenic DI
- No response to vasopressin
- Defective V2 receptor or
- H2O channel defect
- No easy treatment
- No response to vasopressin
Hormone: Aldosterone
- Released from
- Function
- Released from adrenal cortex
- cells in zona glomerulosa mediate release
- adrenal gland sits on top of kidney
- Mineralcorticoid - regulates ion content
- Regulates plasma Na, K, and body fluid vol
- V. sensitive system
- Released in response to:
- increased plama K - 0.1mM
- decreased plasma Na (minor - conc maintained by osmoregulation)
- decreased ECF vol - via renin-angiotensin
Hormone: Aldosterone
- Acts on
- Causes
Acts on
- Late DT (ENaC)
- Collecting Duct
Causes
- increased reabs of Na
- increased reabs H2O
- Increased secretion of K and H
- get rid of K - easiest in urine
Hormone: Aldosterone
- Genomic action
- Works at level of gene to make changes at cell
Aldosterone => Cytosolic receptor => Nucleus => RNA transcription => Protein synthesis (transport proteins & proton pump)
Hormone: Aldosterone on Principal Cell
Aldosterone => Cytosolic receptor => Nucleus => RNA transcription => Protein synthesis (transport protein)
=>
- Na reabs, K and H secretion
- Slow responding: hormonal regulation
- Time: hrs-days
Hormone: Aldosterone on a-IC
Aldosterone => Cytosolic receptor => Nucleus => RNA transcription => Protein synthesis (transport proteins & proton pump)
H secretion
Liddle’s Syndrome
- hypertension
- high Na reabs even though:
- low aldosterone
- Mutation in Na channel function
- endocytosis of ENaC doesn’t work
- too many ENaC proteins in membrane
- Increased no. of Na channels in principal cell
Pseudohypoaldoteronism
- Low response to aldosterone
- Mineralocorticoid receptor problem: not enough ENaC in membrane
- Salt loss but high aldosterone
- Hypotension
Hormones: Renin-Angiotensin
- Regulates
- Renin release
Regulates:
- body fluid vol
- plasma Na & K
Renin release:
- from macula densa cells in afferent arteriole in juxtaglomerular apparatus (JGA) ( near to glomerular)
- Sympathetic
Hormones: Renin-Angiotensin
Cascade
Most made in lungs b/c high density of blood vessels
Renal hormone integration
Vol vs Osmolality
aldosterone predominates
Maintain normal ECFV at impact of osmolality
