Basolateral Na+/H+ exchange maintains potassium secretion during diminished sodium transport in the rabbit cortical collecting duct

Shigeaki Muto, Shuichi Tsuruoka, Yukio Miyata, Akio Fujimura, Eiji Kusano, WenHui Wang, Donald Seldin, Gerhard Giebisch

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


Stimulation of the basolateral Na+/K+-ATPase in the isolated perfused rabbit cortical collecting duct by raising either bath potassium or lumen sodium increases potassium secretion, sodium absorption and their apical conductances. Here we determined the effect of stimulating Na +/K+-ATPase on potassium secretion without luminal sodium transport. Acutely raising bath potassium concentrations from 2.5 to 8.5 mM, without luminal sodium, depolarized the basolateral membrane and transepithelial voltages while increasing the transepithelial, basolateral and apical membrane conductances of principal cells. Fractional apical membrane resistance and cell pH were elevated. Net potassium secretion was maintained albeit diminished and was still enhanced by raising bath potassium, but was reduced by basolateral ethylisopropylamiloride, an inhibitor of Na+/H+ exchange. Luminal iberitoxin, a specific inhibitor of the calcium-activated big-conductance potassium (BK) channel, impaired potassium secretion both in the presence and absence of luminal sodium. In contrast, iberitoxin did not affect luminal sodium transport. We conclude that basolateral Na+/H + exchange in the cortical collecting duct plays an important role in maintaining potassium secretion during compromised sodium supplies and that BK channels contribute to potassium secretion.

Original languageEnglish (US)
Pages (from-to)25-30
Number of pages6
JournalKidney international
Issue number1
StatePublished - Jan 2009


  • Basolateral Na-K-ATPase
  • Ca-activated big-conductance K channels
  • In vitro microperfusion
  • K transport
  • Principal cell
  • ROMK

ASJC Scopus subject areas

  • Nephrology


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