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This Article Full Text Full Text (PDF) All Versions of this Article: 576/1/163    most recent jphysiol.2006.114876v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Jung, S.-R. Articles by Koh, D.-S. Search for Related Content PubMed PubMed Citation Articles by Jung, S.-R. Articles by Koh, D.-S. Related Collections Cellular

¹ Department of Physics, Pohang University of Science and Technology, Pohang, Republic of Korea
² Department of Life Science, Seoul National University, Seoul, Republic of Korea
³ Department of Physiology & Biophysics
⁴ Department of Medicine, School of Medicine, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, WA 98195, USA

Intracellular calcium concentration ([Ca²⁺]_i) is a key factor controlling secretion from various cell types. We investigated how different patterns of [Ca²⁺]_i signals evoke salt secretion via ion transport mechanisms and mucin secretion via exocytosis in dog pancreatic duct epithelial cells (PDEC). Activation of epithelial P2Y₂ receptors by UTP generated two patterns of [Ca²⁺]_i change: 2–10 µM UTP induced [Ca²⁺]_i oscillations, whereas 100 µM UTP induced a sustained [Ca²⁺]_i increase, both in the micromolar range. As monitored by carbon-fibre amperometry, the sustained [Ca²⁺]_i increase stimulated a larger increase in exocytosis than [Ca²⁺]_i oscillations, despite their similar amplitude. In contrast, patch-clamp recordings revealed that [Ca²⁺]_i oscillations synchronously activated a K⁺ current as efficiently as the sustained [Ca²⁺]_i increase. This K⁺ current was mediated by intermediate-conductance Ca²⁺-activated K⁺ channels (32 pS at –100 mV) which were sensitive to charybdotoxin and resistant to TEA. Activation of these Ca²⁺-dependent K⁺ channels hyperpolarized the plasma membrane from a resting potential of –40 mV to –90 mV, as monitored in perforated whole-cell configuration, in turn enhancing Na⁺-independent, Cl^–-dependent and DIDS-sensitive HCO₃^– secretion, as monitored through changes in intracellular pH. PDEC therefore encode concentrations of purinergic agonists as different patterns of [Ca²⁺]_i changes, which differentially stimulate K⁺ channels, the Cl^––HCO₃^– exchanger, and exocytosis. Thus, in addition to amplitude, the temporal pattern of [Ca²⁺]_i increases is an important mechanism for transducing extracellular stimuli into different physiological effects.

(Received 6 June 2006; accepted after revision 18 July 2006; first published online 20 July 2006)
Corresponding author D.-S. Koh: Department of Physiology and Biophysics, University of Washington, Health Sciences Bldg, Seattle, WA 98195-7290, USA. Email: koh{at}u.washington.edu