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Flashcards in nephron function 2 Deck (20):

describe the similarities and differences between Na+ reabsorption in the proximal tubules compared to the short loop nephrons

similarily, Na+ moves out of the cell by a basolateral Na/K/ATPase transporter creating a higher conc in ECF

In contrast, Na+ moves in by Na/2Cl/K channel
K+ is recycled by ROMK channel
tight junctions so no flow of water passively = hypertonic ECF


describe the importance of the Na/2Cl/K channel

this transporter is the target for the diuretic furosemide


describe the short loop nephron

-only within the outer medulla
-NaCl gradient formed by countercurrent multiplication mechanism
-Allows interstitium to reach a concentration of 600mosm/L


how does the water leave the short loop and where does it go

- leaves via osmosis
- enters vasa recta


what is the significance of the blood flow being counter to the direction of tubular flow

countercurrent exchange system prevents wash out of the gradient
- slow BF favours optimal exchange
- increasing flow can cause a loss of the gradient


describe the concentration and transporters within the early distal convoluted tubule

- tubular fluid leaving the TAL is dilute
- further dilution occurs as the tubular fluid is impermeable to water
- Na/Cl transporter on apical surface (Na/K/ATPase basolateral)


what is the importance of the Na/Cl transporter in the early distal convoluted tubule

this transporter is blocked by thiazide diuretics
- used to treat hypertension & heart failure


name the two cell types present in the late distal convoluted tubule, connecting tubule, and collecting duct

principal cells

intercalated cells


describe the role of principal cells and how they carry this out

reabsorb Na+ via ENaC channel
secrete K+ via ROMK (moves to counterbalance electronegativity created by movement of Na+ out)


why are thiazide diuretic importance in terms of K+

thiazide diuretics block Na/Cl transport causing K+ loss (hypokalemia) as more Na+ stays within the late distal tubule
hypokalemia can cause ventricular arrhythmias


describe the role of aldosterone on principal cells

aldosterone released by adrenal cortex and diffuses into principal cell by binding to a receptor. this receptor goes into the nucleus, binds to DNA and changes targets. Causes ENaC up-regulation, induce more ENaC channels, and more Na/K/ATPases
= more Na+ reabsorbed, more K+ excreted


what drug blocks the affect of aldosterone

Spirolactone (is a weak K+ sparing diuretic)


describe the role of intercalated cells

important for acid-base balance and K+ reabsorption
secrete H+ via H+/ATPase & H+/K/ATPase
H+ secreted is used to reabsorb HCO3- and generate new HCO3-


why do we need to make new bicarbonate

bicarbonate is used to buffer out the acidity of H+ ions however in doing so bicarbonate sources get depleted. To maintain pH more bicarbonate is needed to be reabsorbed and made


describe diffusion trapping and why it occurs

- occurs in the collecting ducts
- as a result of excess H+ (after all HCO3- is reabsorbed) it combines with NH3
because NH3 has no charge it can diffuse freely
NH3 + H+ = NH4+
therefore NH4+ excreted, maximum urine pH 4.5


describe water reabsorption in the collecting ducts

depends on ADH (released from post. pituitary)
- inserts aquaporin channels on apical surface allowing water reabsorption
- high levels of ADH = high water reabsorption & conc urine


describe the passive hypothesis in the inner medulla

1. high levels of ADH causing urea conc to increase in corticol collecting ducts (NOT medulla collecting ducts)

2. ADH down the collecting duct moves water and urea into interstitium (base of LOH)

3. salt conc in the inner medulla (interstitium) drops due to presence of water

4. therefore NaCl moves out of the base of the ascending limb (long loop) into the interstitium via osmosis to counter this

(base of nephron within inner medulla now very concentrated)


describe the role of the vasa recta countercurrent

preserves osmotic gradient and carries away water


what happens in the long loop nephrons when ADH is low

- water isn't reabsorbed so urea doesn't increase
- inner medulla CD still permeable to urea when ADH is low
- if urea interstitium > urea CD then urea will diffuse into CD and be excreted = washout
- ADH low = urea in inner medulla low


Describe the drugs acetazolamide, thiazide, spirolactone, and furosemide?

acetazolamide = Carbonic anhydrase inhibitor (relieves metabolic alkalosis)

furosemide = Na/2Cl/K channel blocker (diuretic)

spirolactone = blocks effect of aldosterone

thiazide = Na/Cl in distal convoluted tubule (diuretic)