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Homeostatic mechanism
•High plasma osmolarity detected
•ADH secretion and thirst promote water reabsorption and concentrate urine
Sodium reabsorption in nephron
•Glomerulus- freely filtered from blood into bowmans capsule, initially high concentration
•PCT- 65-70% reabsorbed by Na/K pump (glucose co-transported), and water follows
•Loop of henle- 25-30% in the ascending limb to create medullary osmotic gradient
•DCT- 5%, reabsorption controlled by aldosterone
•Collecting duct- final 3-5%, controlled by aldosterone, fine tuned based on bodies needs
Role of aldosterone
•Produced by adrenal cortex, specifically zona glomerulosa
•Regulates blood pressure, volume, and electrolyte balance
•Promotes sodium reabsorption and potassium excretion/secretion
•Targets DCT and mainly collecting ducts
How does aldosterone work
•Enters cell by simple diffusion (fat soluble), no need for transport protein
•Increase in intracellular Na+ enters from filtrate through Na+ leak channels located on apical membrane
•Aldosterone allows channels to be open longer
•Sodium potassium pump on basolateral membrane driven by ATP pumps 3 Na+ ions out into bloodstream and 2 K+ ions into cell
•Strong gradient created- high sodium concentration in filtrate, low in cell
•Excess intracellular K+ leaves cell and enters filtrate through leak channels on apical membrane (secretion)
•Increases number of K+ leak channels for secretion
What regulates aldosterone secretion
•RAAS stimulated by low BP / volume / sodium
•ANP, baroreceptors can inhibit or stimulate RAAS
•Stimulated by high blood potassium levels
RAAS system
•Responds to low blood pressure, volume or low sodium levels, detected by macula densa
•Juxtaglomerular cells in the afferent arteriole release renin into bloodstream in response to stimuli
•Renin converts angiotensinogen into angiotensin 1
•Angiotensin 1 is converted to angiotensin 2 by the angiotensin converting enzyme (in lungs)
•Angiotensin 2 acts on zona glomerulosa (adrenal gland) which stimulates aldosterone secretion
•Angiotensin 2 itself causes vasoconstriction which raises blood pressure
•Aldosterone increases sodium reabsorption and potassium secretion, water follows sodium which also increases its reabsorption
Paracrine feedback
•Release of signalling molecules e.g hormones or growth factors by a cell
•Act on adjacent cells within the same tissue or organ
•E.g macula densa cells act as sensors that monitor fluid flow and indirectly sodium concentration
Macula densa during high fluid flow
•Cells are located in DCT
•High fluid flow indicates high filtration rate which is often associated with high blood pressure or excess sodium
•Release paracrine signals that act on juxtaglomerular cells and inhibit their release of renin
Low fluid flow
•Fluid flow reduced due to low blood pressure or low sodium levels
•Macula densa send signals to juxtaglomerular cells to release renin which activates RAAS
•Promotes sodium and water reabsorption
Atrial natriuretic peptide
•Released by atria of the heart
•Promotes sodium excretion by inhibiting sodium reabsorption in DCT and collecting ducts by decreasing the activity of sodium channels
•Inhibits renin and ADH release
•Causes vasodilation of afferent arteriole and constriction of efferent which increases GFR and thereforee the amount of sodium excreted
Functions and regulation of potassium
•Proper function of nerve and muscle cells, especially heart
•Exchanges with H+ ions in cells which plays a role in maintaining body’s pH balance
•High potassium level are a stimulus for aldosterone release
•Increases activity of Na/K pumps and increases number of potassium leak channels on basolateral membrane to promote potassium excretion
Thirst and salt apetie
•Thirst when osmolarity raises above 280mOsM/L
•Salt apetite when plasma sodium drops