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Robert M Drummond - One of the best experts on this subject based on the ideXlab platform.

  • the cl channel blocker niflumic acid releases ca2 from an intracellular store in rat pulmonary artery smooth muscle cells
    British Journal of Pharmacology, 2003
    Co-Authors: Stuart F Cruickshank, Lynne M Baxter, Robert M Drummond
    Abstract:

    The effect of the Cl− channel blockers niflumic acid (NFA), 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), and anthracene-9-carboxylic acid (A-9-C), on Ca2+ signalling in rat pulmonary artery smooth muscle cells was examined. Intracellular Ca2+ concentration ([Ca2+]i) was monitored with either fura-2 or Fluo-4, and caffeine was used to activate the ryanodine receptor, thereby releasing Ca2+ from the sarcoplasmic reticulum (SR). NFA and NPPB significantly increased basal [Ca2+]i and attenuated the caffeine-induced increase in [Ca2+]i. These Cl− channel blockers also increased the half-time (t1/2) to peak for the caffeine-induced [Ca2+]i transient, and slowed the removal of Ca2+ from the cytosol following application of caffeine. Since DIDS and A-9-C were found to adversely affect fura-2 fluorescence, Fluo-4 was used to monitor intracellular Ca2+ in studies involving these Cl− channel blockers. Both DIDS and A-9-C increased basal Fluo-4 fluorescence, indicating an increase in intracellular Ca2+, and while DIDS had no significant effect on the t1/2 to peak for the caffeine-induced Ca2+ transient, it was significantly increased by A-9-C. In the absence of extracellular Ca2+, NFA significantly increased basal [Ca2+]i, suggesting that the release of Ca2+ from an intracellular store was responsible for the observed effect. Depleting the SR with the combination of caffeine and cyclopiazonic acid prevented the increase in basal [Ca2+]i induced by NFA. Additionally, incubating the cells with ryanodine also prevented the increase in basal [Ca2+]i induced by NFA. These data show that Cl− channel blockers have marked effects on Ca2+ signalling in pulmonary artery smooth muscle cells. Furthermore, examination of the NFA-induced increase in [Ca2+]i indicates that it is likely due to Ca2+ release from an intracellular store, most probably the SR.

  • The Cl− channel blocker niflumic acid releases Ca2+ from an intracellular store in rat pulmonary artery smooth muscle cells
    British Journal of Pharmacology, 2003
    Co-Authors: Stuart F Cruickshank, Lynne M Baxter, Robert M Drummond
    Abstract:

    The effect of the Cl− channel blockers niflumic acid (NFA), 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), and anthracene-9-carboxylic acid (A-9-C), on Ca2+ signalling in rat pulmonary artery smooth muscle cells was examined. Intracellular Ca2+ concentration ([Ca2+]i) was monitored with either fura-2 or Fluo-4, and caffeine was used to activate the ryanodine receptor, thereby releasing Ca2+ from the sarcoplasmic reticulum (SR). NFA and NPPB significantly increased basal [Ca2+]i and attenuated the caffeine-induced increase in [Ca2+]i. These Cl− channel blockers also increased the half-time (t1/2) to peak for the caffeine-induced [Ca2+]i transient, and slowed the removal of Ca2+ from the cytosol following application of caffeine. Since DIDS and A-9-C were found to adversely affect fura-2 fluorescence, Fluo-4 was used to monitor intracellular Ca2+ in studies involving these Cl− channel blockers. Both DIDS and A-9-C increased basal Fluo-4 fluorescence, indicating an increase in intracellular Ca2+, and while DIDS had no significant effect on the t1/2 to peak for the caffeine-induced Ca2+ transient, it was significantly increased by A-9-C. In the absence of extracellular Ca2+, NFA significantly increased basal [Ca2+]i, suggesting that the release of Ca2+ from an intracellular store was responsible for the observed effect. Depleting the SR with the combination of caffeine and cyclopiazonic acid prevented the increase in basal [Ca2+]i induced by NFA. Additionally, incubating the cells with ryanodine also prevented the increase in basal [Ca2+]i induced by NFA. These data show that Cl− channel blockers have marked effects on Ca2+ signalling in pulmonary artery smooth muscle cells. Furthermore, examination of the NFA-induced increase in [Ca2+]i indicates that it is likely due to Ca2+ release from an intracellular store, most probably the SR.

Stuart F Cruickshank - One of the best experts on this subject based on the ideXlab platform.

  • the cl channel blocker niflumic acid releases ca2 from an intracellular store in rat pulmonary artery smooth muscle cells
    British Journal of Pharmacology, 2003
    Co-Authors: Stuart F Cruickshank, Lynne M Baxter, Robert M Drummond
    Abstract:

    The effect of the Cl− channel blockers niflumic acid (NFA), 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), and anthracene-9-carboxylic acid (A-9-C), on Ca2+ signalling in rat pulmonary artery smooth muscle cells was examined. Intracellular Ca2+ concentration ([Ca2+]i) was monitored with either fura-2 or Fluo-4, and caffeine was used to activate the ryanodine receptor, thereby releasing Ca2+ from the sarcoplasmic reticulum (SR). NFA and NPPB significantly increased basal [Ca2+]i and attenuated the caffeine-induced increase in [Ca2+]i. These Cl− channel blockers also increased the half-time (t1/2) to peak for the caffeine-induced [Ca2+]i transient, and slowed the removal of Ca2+ from the cytosol following application of caffeine. Since DIDS and A-9-C were found to adversely affect fura-2 fluorescence, Fluo-4 was used to monitor intracellular Ca2+ in studies involving these Cl− channel blockers. Both DIDS and A-9-C increased basal Fluo-4 fluorescence, indicating an increase in intracellular Ca2+, and while DIDS had no significant effect on the t1/2 to peak for the caffeine-induced Ca2+ transient, it was significantly increased by A-9-C. In the absence of extracellular Ca2+, NFA significantly increased basal [Ca2+]i, suggesting that the release of Ca2+ from an intracellular store was responsible for the observed effect. Depleting the SR with the combination of caffeine and cyclopiazonic acid prevented the increase in basal [Ca2+]i induced by NFA. Additionally, incubating the cells with ryanodine also prevented the increase in basal [Ca2+]i induced by NFA. These data show that Cl− channel blockers have marked effects on Ca2+ signalling in pulmonary artery smooth muscle cells. Furthermore, examination of the NFA-induced increase in [Ca2+]i indicates that it is likely due to Ca2+ release from an intracellular store, most probably the SR.

  • The Cl− channel blocker niflumic acid releases Ca2+ from an intracellular store in rat pulmonary artery smooth muscle cells
    British Journal of Pharmacology, 2003
    Co-Authors: Stuart F Cruickshank, Lynne M Baxter, Robert M Drummond
    Abstract:

    The effect of the Cl− channel blockers niflumic acid (NFA), 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), and anthracene-9-carboxylic acid (A-9-C), on Ca2+ signalling in rat pulmonary artery smooth muscle cells was examined. Intracellular Ca2+ concentration ([Ca2+]i) was monitored with either fura-2 or Fluo-4, and caffeine was used to activate the ryanodine receptor, thereby releasing Ca2+ from the sarcoplasmic reticulum (SR). NFA and NPPB significantly increased basal [Ca2+]i and attenuated the caffeine-induced increase in [Ca2+]i. These Cl− channel blockers also increased the half-time (t1/2) to peak for the caffeine-induced [Ca2+]i transient, and slowed the removal of Ca2+ from the cytosol following application of caffeine. Since DIDS and A-9-C were found to adversely affect fura-2 fluorescence, Fluo-4 was used to monitor intracellular Ca2+ in studies involving these Cl− channel blockers. Both DIDS and A-9-C increased basal Fluo-4 fluorescence, indicating an increase in intracellular Ca2+, and while DIDS had no significant effect on the t1/2 to peak for the caffeine-induced Ca2+ transient, it was significantly increased by A-9-C. In the absence of extracellular Ca2+, NFA significantly increased basal [Ca2+]i, suggesting that the release of Ca2+ from an intracellular store was responsible for the observed effect. Depleting the SR with the combination of caffeine and cyclopiazonic acid prevented the increase in basal [Ca2+]i induced by NFA. Additionally, incubating the cells with ryanodine also prevented the increase in basal [Ca2+]i induced by NFA. These data show that Cl− channel blockers have marked effects on Ca2+ signalling in pulmonary artery smooth muscle cells. Furthermore, examination of the NFA-induced increase in [Ca2+]i indicates that it is likely due to Ca2+ release from an intracellular store, most probably the SR.

Lynne M Baxter - One of the best experts on this subject based on the ideXlab platform.

  • the cl channel blocker niflumic acid releases ca2 from an intracellular store in rat pulmonary artery smooth muscle cells
    British Journal of Pharmacology, 2003
    Co-Authors: Stuart F Cruickshank, Lynne M Baxter, Robert M Drummond
    Abstract:

    The effect of the Cl− channel blockers niflumic acid (NFA), 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), and anthracene-9-carboxylic acid (A-9-C), on Ca2+ signalling in rat pulmonary artery smooth muscle cells was examined. Intracellular Ca2+ concentration ([Ca2+]i) was monitored with either fura-2 or Fluo-4, and caffeine was used to activate the ryanodine receptor, thereby releasing Ca2+ from the sarcoplasmic reticulum (SR). NFA and NPPB significantly increased basal [Ca2+]i and attenuated the caffeine-induced increase in [Ca2+]i. These Cl− channel blockers also increased the half-time (t1/2) to peak for the caffeine-induced [Ca2+]i transient, and slowed the removal of Ca2+ from the cytosol following application of caffeine. Since DIDS and A-9-C were found to adversely affect fura-2 fluorescence, Fluo-4 was used to monitor intracellular Ca2+ in studies involving these Cl− channel blockers. Both DIDS and A-9-C increased basal Fluo-4 fluorescence, indicating an increase in intracellular Ca2+, and while DIDS had no significant effect on the t1/2 to peak for the caffeine-induced Ca2+ transient, it was significantly increased by A-9-C. In the absence of extracellular Ca2+, NFA significantly increased basal [Ca2+]i, suggesting that the release of Ca2+ from an intracellular store was responsible for the observed effect. Depleting the SR with the combination of caffeine and cyclopiazonic acid prevented the increase in basal [Ca2+]i induced by NFA. Additionally, incubating the cells with ryanodine also prevented the increase in basal [Ca2+]i induced by NFA. These data show that Cl− channel blockers have marked effects on Ca2+ signalling in pulmonary artery smooth muscle cells. Furthermore, examination of the NFA-induced increase in [Ca2+]i indicates that it is likely due to Ca2+ release from an intracellular store, most probably the SR.

  • The Cl− channel blocker niflumic acid releases Ca2+ from an intracellular store in rat pulmonary artery smooth muscle cells
    British Journal of Pharmacology, 2003
    Co-Authors: Stuart F Cruickshank, Lynne M Baxter, Robert M Drummond
    Abstract:

    The effect of the Cl− channel blockers niflumic acid (NFA), 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), and anthracene-9-carboxylic acid (A-9-C), on Ca2+ signalling in rat pulmonary artery smooth muscle cells was examined. Intracellular Ca2+ concentration ([Ca2+]i) was monitored with either fura-2 or Fluo-4, and caffeine was used to activate the ryanodine receptor, thereby releasing Ca2+ from the sarcoplasmic reticulum (SR). NFA and NPPB significantly increased basal [Ca2+]i and attenuated the caffeine-induced increase in [Ca2+]i. These Cl− channel blockers also increased the half-time (t1/2) to peak for the caffeine-induced [Ca2+]i transient, and slowed the removal of Ca2+ from the cytosol following application of caffeine. Since DIDS and A-9-C were found to adversely affect fura-2 fluorescence, Fluo-4 was used to monitor intracellular Ca2+ in studies involving these Cl− channel blockers. Both DIDS and A-9-C increased basal Fluo-4 fluorescence, indicating an increase in intracellular Ca2+, and while DIDS had no significant effect on the t1/2 to peak for the caffeine-induced Ca2+ transient, it was significantly increased by A-9-C. In the absence of extracellular Ca2+, NFA significantly increased basal [Ca2+]i, suggesting that the release of Ca2+ from an intracellular store was responsible for the observed effect. Depleting the SR with the combination of caffeine and cyclopiazonic acid prevented the increase in basal [Ca2+]i induced by NFA. Additionally, incubating the cells with ryanodine also prevented the increase in basal [Ca2+]i induced by NFA. These data show that Cl− channel blockers have marked effects on Ca2+ signalling in pulmonary artery smooth muscle cells. Furthermore, examination of the NFA-induced increase in [Ca2+]i indicates that it is likely due to Ca2+ release from an intracellular store, most probably the SR.

Chris D. Geddes - One of the best experts on this subject based on the ideXlab platform.

  • metal enhanced fluorescence based calcium detection greater than 100 fold increase in signal noise using fluo 3 or fluo 4 and silver nanostructures
    Sensors and Actuators B-chemical, 2011
    Co-Authors: Nina Bondre, Yongxia Zhang, Chris D. Geddes
    Abstract:

    Abstract In this paper we describe metal-enhanced fluorescence (MEF) of the Ca 2+ indicators: Fluo-3 and Fluo-4 in close proximity to silver nano-particles, SiFs. When the concentration of Ca 2+ increases, the MEF enhancement factor decreases, which is consistent with our previous findings that the greatest fluorescence enhancements occur for fluorophores with the lowest free-space quantum yield. Over 100-fold enhanced fluorescence intensities (signal/noise) were observed. In addition, the photostability of the fluorophore (Fluo-3) is much more prolonged from the SIFs as compared to glass (a control sample). Our findings strongly suggest the widespread use and the general approach of nanoparticulate SiFs surfaces for the enhanced detection of both intra and extra-cellular calcium and indeed other analytes of interest.

  • Metal-enhanced fluorescence based calcium detection: Greater than 100-fold increase in signal/noise using Fluo-3 or Fluo-4 and silver nanostructures
    Sensors and Actuators B: Chemical, 2011
    Co-Authors: Nina Bondre, Yongxia Zhang, Chris D. Geddes
    Abstract:

    Abstract In this paper we describe metal-enhanced fluorescence (MEF) of the Ca 2+ indicators: Fluo-3 and Fluo-4 in close proximity to silver nano-particles, SiFs. When the concentration of Ca 2+ increases, the MEF enhancement factor decreases, which is consistent with our previous findings that the greatest fluorescence enhancements occur for fluorophores with the lowest free-space quantum yield. Over 100-fold enhanced fluorescence intensities (signal/noise) were observed. In addition, the photostability of the fluorophore (Fluo-3) is much more prolonged from the SIFs as compared to glass (a control sample). Our findings strongly suggest the widespread use and the general approach of nanoparticulate SiFs surfaces for the enhanced detection of both intra and extra-cellular calcium and indeed other analytes of interest.

Nina Bondre - One of the best experts on this subject based on the ideXlab platform.

  • metal enhanced fluorescence based calcium detection greater than 100 fold increase in signal noise using fluo 3 or fluo 4 and silver nanostructures
    Sensors and Actuators B-chemical, 2011
    Co-Authors: Nina Bondre, Yongxia Zhang, Chris D. Geddes
    Abstract:

    Abstract In this paper we describe metal-enhanced fluorescence (MEF) of the Ca 2+ indicators: Fluo-3 and Fluo-4 in close proximity to silver nano-particles, SiFs. When the concentration of Ca 2+ increases, the MEF enhancement factor decreases, which is consistent with our previous findings that the greatest fluorescence enhancements occur for fluorophores with the lowest free-space quantum yield. Over 100-fold enhanced fluorescence intensities (signal/noise) were observed. In addition, the photostability of the fluorophore (Fluo-3) is much more prolonged from the SIFs as compared to glass (a control sample). Our findings strongly suggest the widespread use and the general approach of nanoparticulate SiFs surfaces for the enhanced detection of both intra and extra-cellular calcium and indeed other analytes of interest.

  • Metal-enhanced fluorescence based calcium detection: Greater than 100-fold increase in signal/noise using Fluo-3 or Fluo-4 and silver nanostructures
    Sensors and Actuators B: Chemical, 2011
    Co-Authors: Nina Bondre, Yongxia Zhang, Chris D. Geddes
    Abstract:

    Abstract In this paper we describe metal-enhanced fluorescence (MEF) of the Ca 2+ indicators: Fluo-3 and Fluo-4 in close proximity to silver nano-particles, SiFs. When the concentration of Ca 2+ increases, the MEF enhancement factor decreases, which is consistent with our previous findings that the greatest fluorescence enhancements occur for fluorophores with the lowest free-space quantum yield. Over 100-fold enhanced fluorescence intensities (signal/noise) were observed. In addition, the photostability of the fluorophore (Fluo-3) is much more prolonged from the SIFs as compared to glass (a control sample). Our findings strongly suggest the widespread use and the general approach of nanoparticulate SiFs surfaces for the enhanced detection of both intra and extra-cellular calcium and indeed other analytes of interest.