ArticleThe Biochemical journal1995
Role of cyclic GMP in the control of capacitative Ca2+ entry in rat pancreatic acinar cells.
Article in The Biochemical journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 36 citations in OpenAlex.
- The functions of store-operated calcium channels.Biochimica et biophysica acta. Molecular cell research · 2017Review
- Protein kinases modulate store-operated channels in pulmonary artery smooth muscle cells.Journal of biomedical science · 2011Article
- ATP depletion induces translocation of STIM1 to puncta and formation of STIM1-ORAI1 clusters: translocation and re-translocation of STIM1 does not require ATP.Pflugers Archiv : European journal of physiology · 2008Article
- Calcium-dependent release of NO from intracellular S-nitrosothiols.The EMBO journal · 2006Article
- Free radicals and the pancreatic acinar cells: role in physiology and pathology.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2005Review
- Inhibition of capacitative calcium entry is not obligatory for relaxation of the mouse anococcygeus by the NO/cyclic GMP signalling pathway.British journal of pharmacology · 2001Article
- Distribution of nitric oxide synthase and secretory role of exogenous nitric oxide in the isolated rat pancreas.International journal of pancreatology : official journal of the International Association of Pancreatology · 2001Article
- Emptying of intracellular Ca2+ stores stimulates Ca2+ entry in mouse pancreatic beta-cells by both direct and indirect mechanisms.The Journal of physiology · 1997Article
- On the molecular basis and regulation of cellular capacitative calcium entry: roles for Trp proteins.Proceedings of the National Academy of Sciences of the United States of America · 1996Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
We have investigated the possible roles of cyclic GMP (cGMP) in initiating or regulating capacitiative Ca2+ entry in rat pancreatic acinar cells. In medium containing 1.8 mM external Ca2+, thapsigargin activated Ca2+ entry and slightly but significantly increased intracellular cGMP concentration. This rise in cGMP levels was prevented by pretreating the cells with the guanylate cyclase inhibitor, LY-83583, or by omitting Ca2+ during stimulation by thapsigargin or methacholine. LY-83583 and NG-nitro-L-arginine (L-NA, an inhibitor of NO synthase) both had a small inhibitory effect on Ca2+ entry when they were added after thapsigargin in Ca2(+)-containing medium, and they reduced by 32 and 48% respectively the thapsigargin-induced capacitative Ca2+ entry when added to the cells during a 20 min preincubation period. However, neither dibutyryl cGMP (Bt2cGMP) nor sodium nitroprusside, an NO mimic, affected either basal intracellular Ca2+ concentration [Ca2+]i or thapsigargin-induced capacitative Ca2+ entry. Further, the inhibitory effects observed after preincubation with LY-83583 or L-NA could not be prevented by preincubation with Bt2cGMP, nor could they be reversed by adding Bt2cGMP, 8-bromo-cGMP or sodium nitroprusside acutely after activation of capacitative Ca2+ entry by thapsigargin. Finally, pretreatment of cells with LY-83583 or L-NA did not affect Ca2+ signalling in response to 1 microM methacholine, including the pattern of [Ca2+]i oscillations. In conclusion, in pancreatic acinar cells, the rise in cellular cGMP levels appears to depend on, rather than cause, the increase in [Ca2+]i with agonist stimulation.
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