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Na-P-i cotransporter type I activity causes a transient intracellular alkalinization during ATP depletion in rabbit medullary thick ascending limb cells

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Abstract
The cellular pathophysiology of renal ischemia-reperfusion injury was investigated in primary cell cultures from rabbit medullary thick ascending limb (MTAL). Metabolic inhibition (MI) was achieved with cyanide and 2-deoxy-glucose. Sixty minutes of MI caused a profound but reversible decrease in intracellular concentration of ATP ([ATP](i)). Intracellular pH (pH(i)) first decreased after initiation of MI, followed by a transient alkalinization. When [ATP](i) reached its lowest value (<1% of control), the cells slowly acidified to reach a stable pH(i) of 6.92 after 50 min of MI. In the presence of EIPA (10 mu mol/L), the pattern of changes in pH(i) was unchanged and acidification was not increased, indicating that the Na+/H+ exchangers were inactive during ATP depletion. When inorganic phosphate (P-i) or Na+ was omitted from the apical solutions during MI, the transient alkalinization was no longer observed and the cytosol slowly acidified. Experiments on Na+-dependent alkalinizations revealed the presence of a Na-P-i cotransporter in the apical cell membrane. With indirect immunofluorescence, the Na-P-i cotransporter expressed in these primary cell cultures could be identified as Na-P-i type I. Although the exact physiological role of Na-P-i type I still is unresolved, these experiments demonstrate that apical Na-P-i type I activity is increased at the onset of ATP depletion in MTAL cells.
Keywords
Author Keywords: MTAL, cell culture, ischemia, metabolic inhibition, alkalinization, intracellular pH, Na-P-i cotransporter, KeyWords Plus: ACUTE PHOSPHATE-DEPLETION, KIDNEY PROXIMAL TUBULES, HENLES LOOP, ISCHEMIA-REPERFUSION, EARLY PHASE, PRIMARY CULTURES, MAGNETIC-RESONANCE, TRANSPORT, LOCALIZATION, EXPRESSION

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Chicago
Jans, F, M Ameloot, Patrick Wouters, and P. Steels. 2008. “Na-P-i Cotransporter Type I Activity Causes a Transient Intracellular Alkalinization During ATP Depletion in Rabbit Medullary Thick Ascending Limb Cells.” Canadian Journal of Physiology and Pharmacology 86 (1-2): 36–45.
APA
Jans, F., Ameloot, M., Wouters, P., & Steels, P. (2008). Na-P-i cotransporter type I activity causes a transient intracellular alkalinization during ATP depletion in rabbit medullary thick ascending limb cells. CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, 86(1-2), 36–45. Presented at the Meeting of the Institute of Circulatory and Respiratory Health.
Vancouver
1.
Jans F, Ameloot M, Wouters P, Steels P. Na-P-i cotransporter type I activity causes a transient intracellular alkalinization during ATP depletion in rabbit medullary thick ascending limb cells. CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY. BUILDING M 55, OTTAWA, ON K1A 0R6, CANADA: NATL RESEARCH COUNCIL CANADA-N R C RESEARCH PRESS,; 2008;86(1-2):36–45.
MLA
Jans, F et al. “Na-P-i Cotransporter Type I Activity Causes a Transient Intracellular Alkalinization During ATP Depletion in Rabbit Medullary Thick Ascending Limb Cells.” CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY 86.1-2 (2008): 36–45. Print.
@article{601073,
  abstract     = {The cellular pathophysiology of renal ischemia-reperfusion injury was investigated in primary cell cultures from rabbit medullary thick ascending limb (MTAL). Metabolic inhibition (MI) was achieved with cyanide and 2-deoxy-glucose. Sixty minutes of MI caused a profound but reversible decrease in intracellular concentration of ATP ([ATP](i)). Intracellular pH (pH(i)) first decreased after initiation of MI, followed by a transient alkalinization. When [ATP](i) reached its lowest value (<1% of control), the cells slowly acidified to reach a stable pH(i) of 6.92 after 50 min of MI. In the presence of EIPA (10 mu mol/L), the pattern of changes in pH(i) was unchanged and acidification was not increased, indicating that the Na+/H+ exchangers were inactive during ATP depletion. When inorganic phosphate (P-i) or Na+ was omitted from the apical solutions during MI, the transient alkalinization was no longer observed and the cytosol slowly acidified. Experiments on Na+-dependent alkalinizations revealed the presence of a Na-P-i cotransporter in the apical cell membrane. With indirect immunofluorescence, the Na-P-i cotransporter expressed in these primary cell cultures could be identified as Na-P-i type I. Although the exact physiological role of Na-P-i type I still is unresolved, these experiments demonstrate that apical Na-P-i type I activity is increased at the onset of ATP depletion in MTAL cells.},
  author       = {Jans, F and Ameloot, M and Wouters, Patrick and Steels, P.},
  issn         = {0008-4212},
  journal      = {CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY},
  keywords     = {Author Keywords: MTAL,cell culture,ischemia,metabolic inhibition,alkalinization,intracellular pH,Na-P-i cotransporter,KeyWords Plus: ACUTE PHOSPHATE-DEPLETION,KIDNEY PROXIMAL TUBULES,HENLES LOOP,ISCHEMIA-REPERFUSION,EARLY PHASE,PRIMARY CULTURES,MAGNETIC-RESONANCE,TRANSPORT,LOCALIZATION,EXPRESSION},
  language     = {eng},
  location     = {Toronto, CANADA, JUN 05-06, 2007},
  number       = {1-2},
  pages        = {36--45},
  publisher    = {NATL RESEARCH COUNCIL CANADA-N R C RESEARCH PRESS,},
  title        = {Na-P-i cotransporter type I activity causes a transient intracellular alkalinization during ATP depletion in rabbit medullary thick ascending limb cells},
  url          = {http://dx.doi.org/10.1139/Y07-114},
  volume       = {86},
  year         = {2008},
}

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