tubular reaborption Flashcards
name the functions and locations of aquaporin-1, aquaporin-2 and aquaporin-3
Aquaporin-1: wide spread and on renal tubules
Aquaporin-2: present in apical membranes of collecting tubule cells. Controlled by ADH
Aquaporin-3: present in basolateral membranes of collecting tubule cells.
What is the ENaC channel? Where is it found? How is it closed and opened?
Sodium and Calcium channel. Found on the apical membrane of nephron cells
Closed by drug amiloride
Opened by a number hormones
What two mechanisms are used to transport Na+ through tubular epithelial cells?
Cell moves Na+ by ATPase and Na+ also moves towards the cell because of the -70mV charge
glucose transporters, an example of secondary active transportinthe kidneys, are responcible for how much glucose reabsorption? What kinds are there? How do they work?
There’s SGLT1 and SGLT2.
SGLT1 reabsorbs 10% of glucose
SGLT2 reabsorbs 90% of glucose
One exchanges glucose for Na+ on the tubular lumen and on the interstitial fluid side the GLUT transporter is run on energy from the ATPase
What substances are actively secreted into the renal tubules?
Creating and para-aminohippuric
What is transport maximum? What is glucose’s transport maximum for glucose?
The transport maximum is the limit of the rate a solute can be transported. The transport maximum is determined by the saturation of a specific transport system.
Max for glucose reabsorption is 375 mg/min
Filtered load for glucose is 125 mg/min
GFR x plasma glucose is 125 ml/min x 1 mg/ml
Anything that exceed the maximum will fail to be reabsorbed and be excreted in the urine.
Why do some passively reabsorbed substances lack a transport maximum?
The rate of diffusion is determined by the electrochemical gradient of the substance
The membrane is permeable to the substance
How long fluid containing the substance is in the tubule effects whether or not there is a transport max. (Which is dependent on the tubular flow rate)
Transport characteristics of the proximal tubule and what molecules/ions and the direction they are transported in?
Highly metabolic and a lot of mitochondria
Has extensive brush borders on the luminal surface
Extensive intercellular and basal channels on interstitial surfaces
Reabsorbed 65% of filtered sodium, chloride, bicarbonate and potassium
All glucose and amino acids
Secretes: organic acids, bases and hydrogen ions
Loop of henle
Has thin and thick segment, ascending and descending
Thin descending is high permeable to water, ~20% of filtered water
Thin ascending is impermeable to water
Thick ascending is also impermeable to water, Na+K+ATPase in basolateral membranes. Sodium-potassium-chloride transporter: 1:2:1. K+ leaks back in which helps move Mg++ and Ca++ out the tubule to the interstitial fluid
What are the loop diuretics?
Furosemide
Ethacrynic acid
Bumetanide
Works on the Na-Cl-K cotransporters
How does the distal tubule work?
Part forms the macula densa
Reabsorbs most ions, impermeable to water and urea
Luminal membrane: Na+Cl- co-transporter - inhibited by thiazide (increases urine output)
basolateral membrane: Na+K+ ATPase pump
What are principal and intercalated cells and where do you find them inthe renal system?
Principal cells reabsorbed Na+ and water fro mthe tube. Secrete K+ into the tube. -sodium-pot pump.
Site of K+ sparing diuretics:
(Spironolactone, eplerenone,) aldostrone agonist (amiloride, trimeterene) Na+ channel blockers
Intercalated cells: reabsorbs K+ and H+ from the tube. by H+ ATPase, protons generated by carbonic anhydrase, and bicarbonate absorbtion.
Found on late distal tubule
Medullary collecting duct
Cuboidal epithelil cells have smooth surfaces and little mitochondria
Water permeability is controlled by ADH
Urea transporter allow permeability to urea
Secretes H+ against large conc
Aldosterone
Source: adrenal cortex
Function: increases sodium reabsorption and stimulates potassium secretion
-sodium=pot pump on basolateral side
Acts on the principal cells of the cortical collecting ducts
What stimulates the secretion of aldosterone, what happens in the absense of and hypersecretion of aldostrone?
Stimulus: increased extracellular potassium and increased levels of angiotensin II
Absense: addison’s disease, causes marked loss of sodium and accumulation of potassium
Hypersecretion: conn’s syndrome