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Cyclosporine stimulates Na+-K+-Cl- cotransport activity in cultured mouse medullary thick ascending limb cells

M S Wu1, C W Yang, M Bens

  • 1Division of Nephrology, Chang Gung Memorial Hospital, Taipei, Taiwan. maisuwu@ms9.hinet.net

Kidney International
|September 30, 2000
PubMed
Abstract

Insights

Cyclosporine (CsA) alters kidney cell transport by inhibiting Na+,K+-ATPase and stimulating Na+-K+-Cl- cotransport. This immunosuppressant may also affect apical potassium recycling in mouse TAL cells.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Physiology

Background:

  • Cyclosporine (CsA) is known to affect plasma membrane transporter activity in kidney epithelial cells.
  • Investigating CsA's impact on Na+,K+-ATPase and Na+-K+-Cl- cotransport in mouse medullary thick ascending limb (mTAL) cells is crucial for understanding its renal effects.

Purpose of the Study:

  • To investigate the effects of Cyclosporine (CsA) on Na+,K+-ATPase and Na+-K+-Cl- cotransport activities.
  • To elucidate the mechanisms by which CsA influences ion transport in cultured mouse mTAL cells.

Main Methods:

  • Experiments utilized cultured mouse mTAL cells expressing mNKCC2 and ROMK channels.
  • Ion transport was assessed using rubidium (86Rb+) and chloride (36Cl-) tracers to measure influx and efflux.
  • Western blotting confirmed the presence of ROMK protein.

Main Results:

  • CsA inhibited Na+,K+-ATPase activity by 38% and increased Na+-K+-Cl- cotransport activity by 38%.
  • CsA stimulated basolateral chloride efflux, which was blocked by NPPB.
  • Apical potassium channel blockade partially prevented CsA-induced chloride efflux and cotransporter stimulation.

Conclusions:

  • CsA stimulates Na+-K+-Cl- cotransport activity in mouse mTAL cells.
  • CsA may interfere with apical potassium recycling in this model system.
  • These findings highlight CsA's complex effects on renal ion transport mechanisms.

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