Ammonium carriers in medullary thick ascending limb
| Autor: | Amel Attmane-Elakeb, Hassane Amlal, Maurice Bichara |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Kidney Medulla
Kidney Medullary cavity Sodium-Potassium-Chloride Symporters Vasopressins Physiology Chemistry Cell Membrane Anatomy Models Biological Antiporters Quaternary Ammonium Compounds chemistry.chemical_compound medicine.anatomical_structure Carrier protein TheoryofComputation_ANALYSISOFALGORITHMSANDPROBLEMCOMPLEXITY Renal medulla medicine Animals Ammonium Carrier Proteins Cation Transport Proteins |
| Zdroj: | American Journal of Physiology-Renal Physiology. 280:F1-F9 |
| ISSN: | 1522-1466 1931-857X |
| Popis: | 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+/NH3in 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 NH3diffusion 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. |
| Databáze: | OpenAIRE |
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