The thick ascending limb of the rat influences urinary net acid excretion by reabsorbing both bicarbonate and ammonium. The bicarbonate absorption is mediated predominantly by apical membrane Na+-H+ exchange and occurs at rates that are comparable to or greater than rates measured in cortical and medullary collecting ducts. The ammonium absorption is mediated predominantly by apical membrane Na+-NH4 +-2Cl- cotransport and enhances urinary ammonium excretion by promoting countercurrent multiplication of ammonium, which facilitates ammonium secretion into medullary collecting ducts. Studies with medullary thick ascending limbs (MTAL) in vitro have shown that the regulation of these transport processes involves both acute responses to changes in the luminal and peritubular environment and adaptive changes in tubule transport capacity in response to chronic systemic acid-base perturbations. In particular, an increase in potassium concentration inhibits ammonium absorption with no effect on net bicarbonate absorption whereas vasopressin inhibits bicarbonate absorption with no effect on net ammonium absorption. Chronic metabolic acidosis causes an adaptive increase in the ability of the MTAL to reabsorb both bicarbonate and ammonium. These results demonstrate that the MTAL is a site of regulation of renal acid-base transport and that ammonium and bicarbonate transport rates can vary independently in this nephron segment.
|Original language||English (US)|
|Number of pages||5|
|Journal||American Journal of Kidney Diseases|
|State||Published - 1989|
ASJC Scopus subject areas
Research output: Contribution to journal › Article