• intracellular [Na+] is kept low by the action of the Na+/K+ATPase pumps in the basolateral membrane. • In the lumen of the renal tubule the H+ combines with filtered HCO3 to form carbonic acid. The HCO3 formed inside the cell by the CA catalyzed RXN moves from the cell into the peritubular fluid either by cotransport with Na+ or counter transport with Cl-. The net effect for HCO3 is reabsorption. Overall, these RXNs in the PT have 3 effects: • Under normal conditions 80 – 90% of the filtered HCO3 is reabsorbed. • H+ is secreted (and, thus excreted) . • Na+ is reabsorbed Late DT and CD This HCO3- is NOT being reabsorbed. It was never in the tubular fluid . it is newly synthesized in the intercalated epithelial cell. Secreted H+ decreases pH of tubular fluid. This cannot decrease past 4.5 because the H+ transporter cannot move past such a strong electrochemical gradient. To minimize pH H+ is buffered with HPO4 -- H2PO4- In the PT buffer is HCO3- , but at this point it has been reabsorbed. Only occurs in cases of severe acidosis and other mechanisms cannot compensate for increase plasma H+ conc. In the PCT glutamine is transported from both the tubular and peritubular fluid into the epithelial cell. Catabolized yielding HCO3- and ammonia. HC03- is not reabsorbed, it was just synthesized. Overall effect: HCO3- added to plasma and a H+ is secreted in the form of NH4+ For blood pH to be normal , ratio of bicarbonate to plasma CO2 must be regulated 20:1. Kidneys regulate HCO3- and respiratory system regulates concentration of CO2
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