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Pattern of Ca2+ increase determines the type of secretory mechanism activated in dog pancreatic duct epithelial cells.

Pattern of Ca2+ increase determines the type of secretory mechanism activated in dog pancreatic duct epithelial cells. Research Abstract Details 

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  • Pattern of Ca2+ increase determines the type of secretory mechanism activated in dog pancreatic duct epithelial cells. Abstract Text:

    seung-ryoung jungSeung-Ryoung Jung,kyungjin kimKyungjin Kim,bertil hilleBertil Hille,toan d nguyenToan D Nguyen,duk-su kohDuk-Su Koh,

    Intracellular calcium concentration ([Ca(2+)](i)) is a key factor controlling secretion from various cell types. We investigated how different patterns of [Ca(2+)](i) signals evoke salt secretion via ion transport mechanisms and mucin secretion via exocytosis in dog pancreatic duct epithelial cells (PDEC). Activation of epithelial P2Y(2) receptors by UTP generated two patterns of [Ca(2+)](i) change: 2-10 microm UTP induced [Ca(2+)](i) oscillations, whereas 100 microm UTP induced a sustained [Ca(2+)](i) increase, both in the micromolar range. As monitored by carbon-fibre amperometry, the sustained [Ca(2+)](i) increase stimulated a larger increase in exocytosis than [Ca(2+)](i) oscillations, despite their similar amplitude. In contrast, patch-clamp recordings revealed that [Ca(2+)](i) oscillations synchronously activated a K(+) current as efficiently as the sustained [Ca(2+)](i) increase. This K(+) current was mediated by intermediate-conductance Ca(2+)-activated K(+) channels (32 pS at -100 mV) which were sensitive to charybdotoxin and resistant to TEA. Activation of these Ca(2+)-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 HCO(3)(-) secretion, as monitored through changes in intracellular pH. PDEC therefore encode concentrations of purinergic agonists as different patterns of [Ca(2+)](i) changes, which differentially stimulate K(+) channels, the Cl(-)-HCO(3)(-) exchanger, and exocytosis. Thus, in addition to amplitude, the temporal pattern of [Ca(2+)](i) increases is an important mechanism for transducing extracellular stimuli into different physiological effects.

    Pattern of Ca2+ increase determines the type of secretory mechanism activated in dog pancreatic duct epithelial cells. Publishing Authors By Initials

    sr jungSR Jung,k kimK Kim,b hilleB Hille,td nguyenTD Nguyen,ds kohDS Koh,

    For similar heterocyclic compounds: heterocyclic compounds, 1-ring: pyrimidines: pyrimidine nucleotides: uracil nucleotides: uridine triphosphate research abstracts see: heterocyclic compounds: heterocyclic compounds, 1-ring: pyrimidines: pyrimidine nucleotides: uracil nucleotides: uridine triphosphate research

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    Pattern of Ca2+ increase determines the type of secretory mechanism activated in dog pancreatic duct epithelial cells. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: The Journal of physiology

    VOLUME: 576

    Page Numbers: 163-78

    Journal Abbreviation: J. Physiol. (Lond.)

    ISSN: 0022-3751

    DAY: 20

    MONTH: 07

    YEAR: 2006

    Pattern of Ca2+ increase determines the type of secretory mechanism activated in dog pancreatic duct epithelial cells. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 266262

    Pattern of Ca2+ increase determines the type of secretory mechanism activated in dog pancreatic duct epithelial cells. Keywords Mesh Terms:

    KEYWORDS: Uridine Triphosphate

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Pattern of Ca2+ increase determines the type of secretory mechanism activated in dog pancreatic duct epithelial cells. Information

    Substance Name: Calcium

    Registry Number: 7440-70-2

    Grant and Affiliation Information for Pattern of Ca2+ increase determines the type of secretory mechanism activated in dog pancreatic duct epithelial cells.

    AFFILIATION: Department of Physiology and Biophysics, University of Washington, Health Sciences Bldg, Seattle, 98195-7290, USA.

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NIDDK

    GRANT: DK55885

    ACRONYM: DK

    MEDLINETA: J Physiol

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