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Nitric oxide induces intracellular Ca 2+ mobilization and increases secretion of incorporated 5‐hydroxytryptamine in rat pancreatic β‐cells
Author(s) -
Willmott Nicholas J.,
Galione Antony,
Smith Paul A.
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00848-4
Subject(s) - thapsigargin , endoplasmic reticulum , intracellular , ryanodine receptor , chemistry , secretion , biophysics , nitric oxide , medicine , endocrinology , microbiology and biotechnology , biochemistry , biology
This study is the first to demonstrate that low concentrations of aqueous NO induce intracellular Ca 2+ mobilization and an increase in secretory activity of rat pancreatic β‐cells. Application of NO solution (2 μM) resulted in a transient increase in the free intracellular Ca 2+ concentration ([Ca 2+ ] i ) of isolated cells, as assessed by video ratio imaging and single wavelength microfluorimetry. Amperometry revealed a simultaneous increase in the release of preloaded 5‐hydroxytryptamine from the isolated cells. The NO‐induced Ca 2+ response primarily involves mobilization of endoplasmic reticulum Ca 2+ stores, since the response was retained when cells were transferred to low Ca 2+ medium, and completely inhibited when cells were pretreated with 10 μM thapsigargin. The Ca 2+ response was also inhibited when cells were incubated with a high concentration of ryanodine (200 μM), suggesting that Ca 2+ mobilization is via a ryanodine‐sensitive store.