What are the driving forces for the proximal tubular H+ and Ca++ transport? The electrochemical gradient for Na+ and/or ATP.
The H+ ion secretion in the proximal tubule as revealed by the reabsorption of the glycodiazine buffer vanishes when the ambient solutions are sodium-free. The same holds for other Na+-dependent transport processes such as Ca++, phosphate, glucose and amino acid reabsorption. If Na+ transport is blocked by ouabain the latter transport processes are abolished, the secretion of H+ ions, however, remains unchanged suggesting H+ to be not exclusively driven by active Na+ transport. These observations agree with electrical measurements which show an electrogenic component of H+ secretion to exist in rat proximal tubule. In experiments with isolated membrane vesicles an electroneutral Na+/H+-exchange mechanism could be demonstrated in the brush border membrane and an ATP-driven Ca++ pumpt as well as Na+-Ca++ countertransport in the baso-lateral cell membrane. These data suggest that both, the Na+ gradient and ATP, are used to drive H+ ion secretion across the luminal brush border and Ca++ reabsorption across the baso-lateral cell side. The biochemical nature of the various systems and their relative importance for the transepithelial ion movement remain to be elucidated.
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D008564:Membrane Potentials; D008871:Microvilli / Q000378:metabolism; D008954:Models, Biological; D010042:Ouabain / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology*
D010042:Ouabain; D000255:Adenosine Triphosphate; D012964:Sodium; D002118:Calcium