ArticleThe Journal of physiology1996
Hypotonic stimulation induced Ca2+ release from IP3-sensitive internal stores in a green monkey kidney cell line.
Article in The Journal of physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 25 citations in OpenAlex.
- Optical single-channel recording of CRAC channels with HaloTag and a CabioRxiv : the preprint server for biology · 2026Article
- Cellular volume regulation by anoctamin 6: Ca²⁺, phospholipase A2 and osmosensing.Pflugers Archiv : European journal of physiology · 2016Article
- G protein modulation of K2P potassium channel TASK-2 : a role of basic residues in the C terminus domain.Pflugers Archiv : European journal of physiology · 2013Article
- TASK-2: a K2P K(+) channel with complex regulation and diverse physiological functions.Frontiers in physiology · 2013Article
- Opposite effects of PSD-95 and MPP3 PDZ proteins on serotonin 5-hydroxytryptamine2C receptor desensitization and membrane stability.Molecular biology of the cell · 2006Article
- Phospholipase C-linked receptors regulate the ATP-sensitive potassium channel by means of phosphatidylinositol 4,5-bisphosphate metabolism.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Hypotonic stimulation (180 +/- 5 mosmol l-1) increased [Ca2+]i in fura-2-loaded Green monkey kidney cells (COS-7 cells) and depolarized the membrane. 2. COS-7 cells were depolarized up to -3.5 +/- 4.4 mV from a resting membrane potential of -35.2 +/- 2.3 mV in response to hypotonic stimulation, when the patch electrode was filled with a 160 mM KCl-0.5 mM EGTA-based intracellular medium. 3. The increase in [Ca2+]i induced by hypotonic stimulation was divided into two phases. One was transient and oscillatory, and observed in Ca(2+)-free medium; the other was persistent, blocked by 100 microM La3+, and observed only in Ca(2+)-containing medium. 4. The increase in [Ca2+]i in Ca(2+)-free medium was blocked by pretreatment with 10 microM thapsigargin. The increase in [Ca2+]i induced by 10 microM thapsigargin was reduced after hypotonic stimulation which induced an increase in [Ca2+]i in Ca(2+)-free medium. 5. The increase in [Ca2+]i in Ca(2+)-free medium was not affected by treatment with 5 mM caffeine or 1-10 microM ryanodine. Neither caffeine nor ryanodine induced an increase in [Ca2+]i. 6. Adenosine 5'-O-2-thiodiphosphate (ADP-beta-S; a P2Y receptor agonist) induced an increase in [Ca2+]i in Ca(2+)-free medium and caused phosphoinositide breakdown in COS-7 cells. Exposure to 10 microM ADP-beta-S blocked the increase in [Ca2+]i induced in the Ca(2+)-free medium by hypotonic stimulation. The results of summary points 4, 5, and 6 suggest that the increase in [Ca2+]i induced by hypotonic stimulation is due to Ca2+ release from inositol 1,4,5-trisphosphate (IP3)-sensitive internal stores. 7. The hypotonic stimulation-activated hydrolysis of phosphoinositides was decreased by pertussis toxin (PTX) in a dose-dependent manner. 8. These observations strongly suggest that hypotonic stimulation induced an increase in [Ca2+]i in Ca(2+)-free medium through activation of cascades using PTX-sensitive guanine nucleotide binding protein (G protein) and IP3.
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