Renal Transport Mechanisms Flashcards
HCO3- Reabsorption
Na+ coupled in the early proximal tubule. Indirect absorption because it does not transverse the apical membrane. The PT secretes H+ which combines with filtered HCO3- to form carbonic acid (H2CO3) which dissociates into CO2 and H20 and is reabsorbed as such. This is catalyzed by carbonic anhydrase. The Na+/H+ transporter is driven by a low [Na] gradient by the Na/K ATPase in the basolateral surface of the cell. The Na/HCO3 brings it from the cell to the blood.
Acetazolamide
Carbonic anhydrase inhibitor. Cannot reabsorb HCO3- and therefore less water escapes the tubules.
Sodium Co-Transporters
Na-Glucose, Na-amino acids, Na-lactate, and Na-inorganic phosphate. Early PT. Increasing ratios of Na to co-transporters in series, increasing the avidity of nutrient reabsorption along the length of Pt.
Cl- in the PT
Anions are reabsorbed along the PT, so the Cl- stays and eventually the concentration difference drives the Cl- out of the tubes through the paracellular pathway. This continued gradient drives out even more Na+ and other cation paracellular later in the tubules.
NaCl Reabsorption in the PT
Second half of the tubule. Apical Na/H and a Cl/Organic Anion exchanger. Basolateral Na/K ATPase creates the gradient for the Na/H. The Cl/organic anion is driven by the higher concentration of the organic anions in the cell. H+ also neutralize the organic anion in the lumen while the resulting cellular alkalinization aids in the dissociation of the acid into anion and H+ in the cell. The neutralized organic acids are lipophilic. Basolateral Na/K-ATPase and K/Cl cotransporter. Nonionic diffusion.
Starling forces in the PT
The rate limiting step is the uptake of fluid from the interstitium to the blood because the apical membrane PT is so leaky. Changes in interstitial hydrostatic pressure and hydrostatic and oncotic pressure in the capillary have a significant impact of rate on fluid reabsorption.
Glomerulotubular Balance
Regulation of salt and water. 1. Increase in filtration increases cotransporters for Na which increases water reabsorption. 2. When GFR changes because of efferent arteriolar tone, changes occur in Starling. 3. Bending of microvilli in the PT sense flow and this stimulates Na transport.
PT hormonal and neural
Angiotensin II- Stimulates the Na/H exchanger. Sympathetic acts directly on PT cells and in severe volume depletion, increased sympathetic increases salt and water retention. Alpha-adrenergic receptors increase the apical Na/H exchanger.
Dopamine
Inhibitor of the PT produced locally by the PT from L-Dopa. This is stimulated by ECFV expansion.
ANP
Stretch in the atria.
Xenobiotics
First line of defense is binding to albumin. This limits their filtration. Taken up actively in the basolateral membrane by high affinity transporters. Cleared at a rate comparable to blood flow. Electrochemical gradients and ATP efflux pumps.
Protein and Oligopeptide in PT
Albumin is endocytosed and degraded and the amino acid are recycled in the blood. Smaller proteins were filtered and degraded into amino acids in the brush border. Renal elimination = metabolic clearance.
Loop of Henle
Indispensable for elaborating both dilute as well as concentrated urine. It reabsorbs 25% of Na but only 15% of filtered water.
Descending Limb
Water reabsorption is restricted. Follows a gradient in the interstitium created by the TAL.
Ascending Limb
First segment in the nephron impermeable to water. Water cannot follow the salt. Salt reabsorption is both transcellular and paracellular. Na/H somewhat. Luminal Na/K/2Cl cotransporter is the main source. Recycle K through an apical K channel. The K+ makes it lumen positive, allowing more sodium reabsorption through paracellular. Also drive Ca++ and Mg++ this way.