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Ammonium carriers in medullary thick ascending limb Attmane-Elakeb A; Amlal H; Bichara MAm J Physiol Renal Physiol 2001[Jan]; 280 (1): F1-9Absorption of NH(4)(+) by the medullary thick ascending limb (MTAL) is a key event in the renal handling of NH(4)(+), leading to accumulation of NH(4)(+)/NH(3) in the renal medulla, which favors NH(4)(+) secretion in medullary collecting ducts and excretion in urine. The Na(+)-K(+)(NH(4)(+))-2Cl(-) cotransporter (BSC1/NKCC2) ensures approximately 50-65% of MTAL active luminal NH(4)(+) uptake under basal conditions. Apical barium- and verapamil-sensitive K(+)/NH(4)(+) antiport and amiloride-sensitive NH(4)(+) conductance account for the rest of active luminal NH(4)(+) transport. The presence of a K(+)/NH(4)(+) antiport besides BSC1 allows NH(4)(+) and NaCl absorption by MTAL to be independently regulated by vasopressin. At the basolateral step, the roles of NH(3) diffusion coupled to Na(+)/H(+) exchange or Na(+)/NH(4)(+) exchange, which favors NH(4)(+) absorption, and of Na(+)/K(+)(NH(4)(+))-ATPase, NH(4)(+)-Cl(-) cotransport, and NH(4)(+) conductance, which oppose NH(4)(+) absorption, have not been quantitatively defined. The increased ability of the MTAL to absorb NH(4)(+) during chronic metabolic acidosis involves an increase in BSC1 expression, but fine regulation of MTAL NH(4)(+) transport probably requires coordinated effects on various apical and basolateral MTAL carriers.|*Cation Transport Proteins[MESH]|Animals[MESH]|Antiporters/*metabolism[MESH]|Carrier Proteins/*metabolism[MESH]|Cell Membrane/physiology[MESH]|Kidney Medulla/*physiology[MESH]|Models, Biological[MESH]|Quaternary Ammonium Compounds/*metabolism[MESH]|Sodium-Potassium-Chloride Symporters[MESH]|Vasopressins/physiology[MESH] |
