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1 Institut National de la Santé et de la Recherche Médicale Médicale Unité 426, Institut Fédératif Régional Xavier Bichat, Faculté de Médecine Xavier Bichat, 75870 Paris Cédex 18, France; and 2 Department of Medicine, Division of Nephrology and Hypertension, University of Cincinnati, Cincinnati, Ohio 45267-0585
Absorption of NH4+ by the medullary thick
ascending limb (MTAL) is a key event in the renal handling of
NH4+, leading to accumulation of
NH4+/NH3 in the renal medulla, which favors
NH4+ secretion in medullary collecting ducts and
excretion in urine. The
Na+-K+(NH4+)-2Cl
cotransporter (BSC1/NKCC2) ensures ~50-65% of MTAL active
luminal NH4+ uptake under basal conditions. Apical
barium- and verapamil-sensitive K+/NH4+
antiport and amiloride-sensitive NH4+ conductance
account for the rest of active luminal NH4+ transport.
The presence of a K+/NH4+ antiport besides
BSC1 allows NH4+ and NaCl absorption by MTAL to be
independently regulated by vasopressin. At the basolateral step, the
roles of NH3 diffusion coupled to
Na+/H+ exchange or
Na+/NH4+ exchange, which favors
NH4+ absorption, and of
Na+/K+(NH4+)-ATPase,
NH4+-Cl cotransport, and
NH4+ conductance, which oppose NH4+
absorption, have not been quantitatively defined. The increased ability
of the MTAL to absorb NH4+ during chronic metabolic
acidosis involves an increase in BSC1 expression, but fine regulation
of MTAL NH4+ transport probably requires coordinated
effects on various apical and basolateral MTAL carriers.
sodium-potassium(ammonium)-2 chloride cotransport; potassium/ammonium(hydrogen) antiport; ammonium conductance; potassium(ammonium)-chloride cotransport; medullary thick ascending limb ammonium transport regulation
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