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Title: Involvement of the ryanodine-sensitive Ca2+ store in GLP-1-induced Ca2+ oscillations in insulin-secreting HIT cells. Author: Sasaki S, Nakagaki I, Kondo H, Hori S. Journal: Pflugers Arch; 2002 Dec; 445(3):342-51. PubMed ID: 12466936. Abstract: We investigated intracellular Ca(2+) ([Ca(2+)](i)) oscillations evoked by glucagon-like peptide 1 (GLP-1) in relation to the ryanodine receptor (RyR) and Ca(2+)-induced Ca(2+)release (CICR) mechanism in pancreatic B cell HIT. GLP-1 produced [Ca(2+)](i) oscillations in the cells, both in media with and without Ca(2+), an effect inhibited by ruthenium red and mimicked by 8-Br-cAMPS. In addition, the GLP-1-evoked [Ca(2+)](i) rise was initiated at the local intercellular peripheral cytoplasm, and a resultant expansion of the intercellular space was also observed. Caffeine induced [Ca(2+)](i) elevation in the medium with or without Ca(2+), an effect inhibited by ruthenium red. GLP-1-evoked [Ca(2+)](i) oscillations were also enhanced by IBMX, and eliminated by Rp-8-Br-cAMPS or 20 microM H-89 treatments whereas they were unaffected by 2 microM H-89 treatment. Forskolin caused a transient elevation in [Ca(2+)](i) that was reduced by Rp-8-Br-cAMPS, 2 microM or 20 microM H-89. Our results indicate that GLP-1 initially generated a local [Ca(2+)](i) elevation at the peripheral cytoplasm, subsequently producing [Ca(2+)](i) oscillations that were inhibited by ruthenium red, involving ryanodine-sensitive and cAMP-activated CICR mechanisms. The cytoplasmic levels of cAMP as well as local Ca(2+) might be responsible for [Ca(2+)](i) oscillations.[Abstract] [Full Text] [Related] [New Search]