Sodium-calcium exchange influences the response to endothelin-1 in lens epithelium

Mansim Okafor, Shigeo Tamiya, Nicholas A. Delamere

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


Studies were conducted to examine the possible involvement of Na+-Ca2+ exchangrr in determining the magnitude of the endothelin-1 (ET-1)-receptor-mediated calcium signal in porcine lens epithelial cells. Cytoplasmic calcium concentration was measured in primary cultured cells loaded with Fura-2. ET-1 (100 nM) caused cytoplasmic calcium to increase transiently to ∼250 nM from a baseline of ∼65 nM. The calcium increase decayed to a sustained plateau 35-45 nM above the baseline. Both the peak and plateau component of the ET-1 calcium response were abolished by PD145065, an ET receptor antagonist, and by cyclopiazonic acid (CPA) (10 μM). In calcium-free bathing solution, only the plateau was abolished. In the presence of ouabain, low-sodium bathing solution or bepridil, a sodium-calcium exchange inhibitor, peak height more than doubled. Bepridil also increased the peak height of the calcium response to ATP. The half-time for decay of the ET-1 and ATP calcium peak was increased several folds by bepridil, ouabain and low-sodium conditions. Measurements of ionomycin-releasable calcium suggested calcium store size was not increased in bepridil-treated cells. Taken together findings suggest inhibition of sodium-calcium exchange increases the magnitude of the receptor-initiated store-release phase of the ET-1 calcium signaling response as the result of impaired calcium clearance from the cytoplasm.

Original languageEnglish (US)
Pages (from-to)231-240
Number of pages10
JournalCell Calcium
Issue number3
StatePublished - Sep 1 2003


  • Bepridil
  • Calcium
  • Endothelin
  • Lens epithelium
  • Na-Ca exchange
  • Ouabain

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology


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