Integration of salt and water balance (use of textbook and slides pls) Flashcards
What happens when you are dehydrated?
Water deficit -> Increase in plasma osmolality -> increase in ADH secretion from posterior pituitary -> increase in plasma ADH -> increase in water permeability in distal tubules and collecting duct -> Increase in water reabsorption -> urine output low and conc.
Where is ADH made and released and due to what being sensed?
primarily in the hypothalamus and released by posterior pituitary
- osmoreceptors sense osmolality (high) (a change in 1%)
- medullary vasomotor centre inputs to hypothalamus when low circulating volume (a change in 10%)
What can be said about the release in ADH in response to a change in osmolality?
If increased, the response has a lower threshold but is more sensitive than to a decrease in ECF volume
What ar some non physiological causes of ADH release?
Pain, stress, drugs, carcinomas.
Alcohol inhibits ADH secretion
How does ADH work at a molecular level?
Binds to V2 receptors on the interstitial fluid side, evoking the placement of AQP-2 (aquaporin) channels on the tubular surface of these distal tubule/ collecting duct cells.
NB via adenylyl cyclase, cAMP and protein kinases
What happens if ADH levels are very low?
central (inability to produce) and nephrogenic (no V2 receptors in the kidney) diabetes insipidus (excessive thirst, large urine amounts)
CDI treated with ADH analogs. To determine which kind, do a water deprivation test, and monitor urine osmolality. Introduce ADH analog and look for change in osmolality.
What is SIADH?
Syndrome of inappropriate ADH secretion.
Retention of water. Low plasma osmolality.
Must limit water intake. Caused by head trauma/ cancers
What cells secrete renin and why?
The granular/JG cells in the afferent arteriole of the JG apparatus.
Released in response to sympathetic stimulation, decreased blood pressure (AA) and a decrease in macula densa NaCl delivery
How does renin work? ** slide from lec 1
Renin cleaves liver made angiotensinogen to angiotensin I -> ACE in the lungs truns AI to AII ->
AT1 receptors: ^aldosterone (adrenal glands), vasoconstriction, ^proximal Na+ reabs, thirst, ADH release, decrease in RBF but maintains GFR
AT2: vasodilation (less of these receptors)
How can this system be blocked?
ACE inhibitors (Altace atacand), ARB’s
What will AII do?
Increase aldosterone
EA constriction
proximal Na+ reabsoprtion (AT1) by upregulating the sodium hydrogen exchanger. (put into ECF by the classic and a Na bicarbonate symport)
What causes aldosterone release?
High potassium and angiotensin II
Where does aldosterone bind?
Principal cells of cortical collecting tubule.
Binds to mineralocorticoid receptor (in cytosol)
causes expression of EnaC channels, eventually causing K+ secretion into tubule (ROMK?)
What two drugs inhibit aldosterone action?
Spironolactone (on MC receptor)
Amiloride ( block EnaC) so is a potassium sparing diuretic
extra, up to 10% of essential hypertension cases are due to hyperaldosetronism
What systems are involved with increasing sodium reabsorption?
RAAS
SNS
ADH (not much)
