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Pierre Pacaud - One of the best experts on this subject based on the ideXlab platform.

  • release of ca2 from Intracellular Store in smooth muscle cells of rat portal vein by atp induced ca2 entry
    British Journal of Pharmacology, 1994
    Co-Authors: Pierre Pacaud, Guillaume Gregoire, Gervaise Loirand
    Abstract:

    Abstract 1. The action of adenosine 5'-triphosphate (ATP, 10 microM) was studied in single patch-clamped smooth muscle cells of rat portal vein where the free internal Ca2+ concentration in the cell (Cai) was estimated by the emission from the dye indo-1. 2. In the presence of 20 microM gallopamil (D600), a blocker of voltage-dependent Ca2+ channels, ATP applied to cells held at a holding potential of -60 mV evoked a transient inward current and an increase in Cai. 3. The rise in Cai evoked by ATP was completely suppressed in the absence of external Ca2+ although a transient inward current was still observed. 4. ATP-induced responses were not modified by the addition of the inositol 1,4,5-trisphosphate receptor antagonist, heparin (1 mM) in the pipette solution. 5. In the presence of caffeine (5 mM) or ryanodine (100 microM) in the pipette solution, which deplete the Intracellular Ca2+ Store, the ATP-induced Cai rise was greatly reduced. 6. Our results suggest that in single cells from rat portal vein, ATP releases Ca2+ from Intracellular Stores without involving InsP3, but via a Ca2+ release mechanism activated by Ca2+ influx through ATP-gated channels.

  • Release of Ca2+ from Intracellular Store in smooth muscle cells of rat portal vein by ATP‐induced Ca2+ entry
    British Journal of Pharmacology, 1994
    Co-Authors: Pierre Pacaud, Guillaume Gregoire, Gervaise Loirand
    Abstract:

    Abstract 1. The action of adenosine 5'-triphosphate (ATP, 10 microM) was studied in single patch-clamped smooth muscle cells of rat portal vein where the free internal Ca2+ concentration in the cell (Cai) was estimated by the emission from the dye indo-1. 2. In the presence of 20 microM gallopamil (D600), a blocker of voltage-dependent Ca2+ channels, ATP applied to cells held at a holding potential of -60 mV evoked a transient inward current and an increase in Cai. 3. The rise in Cai evoked by ATP was completely suppressed in the absence of external Ca2+ although a transient inward current was still observed. 4. ATP-induced responses were not modified by the addition of the inositol 1,4,5-trisphosphate receptor antagonist, heparin (1 mM) in the pipette solution. 5. In the presence of caffeine (5 mM) or ryanodine (100 microM) in the pipette solution, which deplete the Intracellular Ca2+ Store, the ATP-induced Cai rise was greatly reduced. 6. Our results suggest that in single cells from rat portal vein, ATP releases Ca2+ from Intracellular Stores without involving InsP3, but via a Ca2+ release mechanism activated by Ca2+ influx through ATP-gated channels.

  • ca2 and sr2 entry induced ca2 release from the Intracellular ca2 Store in smooth muscle cells of rat portal vein
    The Journal of Physiology, 1993
    Co-Authors: Guillaume Gregoire, Gervaise Loirand, Pierre Pacaud
    Abstract:

    1. Changes in cytosolic free Ca2+ concentration ([Ca2+]i) induced by membrane depolarizations were investigated using indo-1 microspectrofluorimetry in single patch-clamped smooth muscle cells of rat portal vein at room temperature (20-21 degrees C) and in the presence of 2 mM Ca2+. 2. During a 1 s depolarization from -50 to -30 mV [Ca2+]i rose, but, although the Ca2+ current was terminated by repolarization to -50 mV, [Ca2+]i continued to increase in a regenerative manner. The delay between the end of the voltage step and the peak of the [Ca2+]i rise was reduced by increasing the depolarization. 3. When a second identical depolarization was rapidly applied (8-13s) after the first one, it induced an identical Ca2+ current but a smaller increase in [Ca2+]i which started to decay upon repolarization. 4. A low concentration of caffeine (0.05 mM), applied to cells showing a small depolarization-induced [Ca2+]i transient which reached a peak at the end of the voltage step, produced an increase in amplitude and in duration of the [Ca2+]i rise without changing the amplitude of the depolarization-induced Ca2+ current. 5. The depolarization-induced [Ca2+]i rise was shortened and reduced in amplitude after noradrenaline- (NA 10 microM) or caffeine- (5 mM) induced release of Ca2+ Store and when the patch pipette solution contained ryanodine (100 microM). Under these conditions, the depolarization-induced [Ca2+]i transient was maximal at the end of the voltage step and declined immediately when the membrane was repolarized at -50 mV. 6. Experiments were done by replacing extracellular Ca2+ by Sr2+. Depolarization-induced Sr2+ entry through voltage-dependent Ca2+ channels could evoke an increase in indo-1 fluorescence which occurred after the termination of the voltage step. This delayed component of fluorescence increase displayed properties similar to those of the regenerative [Ca2+]i rise recorded in the Ca(2+)-containing solution. 7. The inefficiency of the second of two successive depolarizations to produce the delayed component of [Ca2+]i rise was not due to the emptiness of the Intracellular Ca2+ Store since, under these conditions, caffeine was still able to induce a Ca2+ release. 8. It is concluded that depolarization-evoked Ca2+ or Sr2+ entry through voltage-dependent Ca2+ channels induced the release of Ca2+ from an Intracellular Store, which could occur in a regenerative manner, independent of the termination of the triggering current.

Gervaise Loirand - One of the best experts on this subject based on the ideXlab platform.

  • release of ca2 from Intracellular Store in smooth muscle cells of rat portal vein by atp induced ca2 entry
    British Journal of Pharmacology, 1994
    Co-Authors: Pierre Pacaud, Guillaume Gregoire, Gervaise Loirand
    Abstract:

    Abstract 1. The action of adenosine 5'-triphosphate (ATP, 10 microM) was studied in single patch-clamped smooth muscle cells of rat portal vein where the free internal Ca2+ concentration in the cell (Cai) was estimated by the emission from the dye indo-1. 2. In the presence of 20 microM gallopamil (D600), a blocker of voltage-dependent Ca2+ channels, ATP applied to cells held at a holding potential of -60 mV evoked a transient inward current and an increase in Cai. 3. The rise in Cai evoked by ATP was completely suppressed in the absence of external Ca2+ although a transient inward current was still observed. 4. ATP-induced responses were not modified by the addition of the inositol 1,4,5-trisphosphate receptor antagonist, heparin (1 mM) in the pipette solution. 5. In the presence of caffeine (5 mM) or ryanodine (100 microM) in the pipette solution, which deplete the Intracellular Ca2+ Store, the ATP-induced Cai rise was greatly reduced. 6. Our results suggest that in single cells from rat portal vein, ATP releases Ca2+ from Intracellular Stores without involving InsP3, but via a Ca2+ release mechanism activated by Ca2+ influx through ATP-gated channels.

  • Release of Ca2+ from Intracellular Store in smooth muscle cells of rat portal vein by ATP‐induced Ca2+ entry
    British Journal of Pharmacology, 1994
    Co-Authors: Pierre Pacaud, Guillaume Gregoire, Gervaise Loirand
    Abstract:

    Abstract 1. The action of adenosine 5'-triphosphate (ATP, 10 microM) was studied in single patch-clamped smooth muscle cells of rat portal vein where the free internal Ca2+ concentration in the cell (Cai) was estimated by the emission from the dye indo-1. 2. In the presence of 20 microM gallopamil (D600), a blocker of voltage-dependent Ca2+ channels, ATP applied to cells held at a holding potential of -60 mV evoked a transient inward current and an increase in Cai. 3. The rise in Cai evoked by ATP was completely suppressed in the absence of external Ca2+ although a transient inward current was still observed. 4. ATP-induced responses were not modified by the addition of the inositol 1,4,5-trisphosphate receptor antagonist, heparin (1 mM) in the pipette solution. 5. In the presence of caffeine (5 mM) or ryanodine (100 microM) in the pipette solution, which deplete the Intracellular Ca2+ Store, the ATP-induced Cai rise was greatly reduced. 6. Our results suggest that in single cells from rat portal vein, ATP releases Ca2+ from Intracellular Stores without involving InsP3, but via a Ca2+ release mechanism activated by Ca2+ influx through ATP-gated channels.

  • ca2 and sr2 entry induced ca2 release from the Intracellular ca2 Store in smooth muscle cells of rat portal vein
    The Journal of Physiology, 1993
    Co-Authors: Guillaume Gregoire, Gervaise Loirand, Pierre Pacaud
    Abstract:

    1. Changes in cytosolic free Ca2+ concentration ([Ca2+]i) induced by membrane depolarizations were investigated using indo-1 microspectrofluorimetry in single patch-clamped smooth muscle cells of rat portal vein at room temperature (20-21 degrees C) and in the presence of 2 mM Ca2+. 2. During a 1 s depolarization from -50 to -30 mV [Ca2+]i rose, but, although the Ca2+ current was terminated by repolarization to -50 mV, [Ca2+]i continued to increase in a regenerative manner. The delay between the end of the voltage step and the peak of the [Ca2+]i rise was reduced by increasing the depolarization. 3. When a second identical depolarization was rapidly applied (8-13s) after the first one, it induced an identical Ca2+ current but a smaller increase in [Ca2+]i which started to decay upon repolarization. 4. A low concentration of caffeine (0.05 mM), applied to cells showing a small depolarization-induced [Ca2+]i transient which reached a peak at the end of the voltage step, produced an increase in amplitude and in duration of the [Ca2+]i rise without changing the amplitude of the depolarization-induced Ca2+ current. 5. The depolarization-induced [Ca2+]i rise was shortened and reduced in amplitude after noradrenaline- (NA 10 microM) or caffeine- (5 mM) induced release of Ca2+ Store and when the patch pipette solution contained ryanodine (100 microM). Under these conditions, the depolarization-induced [Ca2+]i transient was maximal at the end of the voltage step and declined immediately when the membrane was repolarized at -50 mV. 6. Experiments were done by replacing extracellular Ca2+ by Sr2+. Depolarization-induced Sr2+ entry through voltage-dependent Ca2+ channels could evoke an increase in indo-1 fluorescence which occurred after the termination of the voltage step. This delayed component of fluorescence increase displayed properties similar to those of the regenerative [Ca2+]i rise recorded in the Ca(2+)-containing solution. 7. The inefficiency of the second of two successive depolarizations to produce the delayed component of [Ca2+]i rise was not due to the emptiness of the Intracellular Ca2+ Store since, under these conditions, caffeine was still able to induce a Ca2+ release. 8. It is concluded that depolarization-evoked Ca2+ or Sr2+ entry through voltage-dependent Ca2+ channels induced the release of Ca2+ from an Intracellular Store, which could occur in a regenerative manner, independent of the termination of the triggering current.

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.

Guillaume Gregoire - One of the best experts on this subject based on the ideXlab platform.

  • release of ca2 from Intracellular Store in smooth muscle cells of rat portal vein by atp induced ca2 entry
    British Journal of Pharmacology, 1994
    Co-Authors: Pierre Pacaud, Guillaume Gregoire, Gervaise Loirand
    Abstract:

    Abstract 1. The action of adenosine 5'-triphosphate (ATP, 10 microM) was studied in single patch-clamped smooth muscle cells of rat portal vein where the free internal Ca2+ concentration in the cell (Cai) was estimated by the emission from the dye indo-1. 2. In the presence of 20 microM gallopamil (D600), a blocker of voltage-dependent Ca2+ channels, ATP applied to cells held at a holding potential of -60 mV evoked a transient inward current and an increase in Cai. 3. The rise in Cai evoked by ATP was completely suppressed in the absence of external Ca2+ although a transient inward current was still observed. 4. ATP-induced responses were not modified by the addition of the inositol 1,4,5-trisphosphate receptor antagonist, heparin (1 mM) in the pipette solution. 5. In the presence of caffeine (5 mM) or ryanodine (100 microM) in the pipette solution, which deplete the Intracellular Ca2+ Store, the ATP-induced Cai rise was greatly reduced. 6. Our results suggest that in single cells from rat portal vein, ATP releases Ca2+ from Intracellular Stores without involving InsP3, but via a Ca2+ release mechanism activated by Ca2+ influx through ATP-gated channels.

  • Release of Ca2+ from Intracellular Store in smooth muscle cells of rat portal vein by ATP‐induced Ca2+ entry
    British Journal of Pharmacology, 1994
    Co-Authors: Pierre Pacaud, Guillaume Gregoire, Gervaise Loirand
    Abstract:

    Abstract 1. The action of adenosine 5'-triphosphate (ATP, 10 microM) was studied in single patch-clamped smooth muscle cells of rat portal vein where the free internal Ca2+ concentration in the cell (Cai) was estimated by the emission from the dye indo-1. 2. In the presence of 20 microM gallopamil (D600), a blocker of voltage-dependent Ca2+ channels, ATP applied to cells held at a holding potential of -60 mV evoked a transient inward current and an increase in Cai. 3. The rise in Cai evoked by ATP was completely suppressed in the absence of external Ca2+ although a transient inward current was still observed. 4. ATP-induced responses were not modified by the addition of the inositol 1,4,5-trisphosphate receptor antagonist, heparin (1 mM) in the pipette solution. 5. In the presence of caffeine (5 mM) or ryanodine (100 microM) in the pipette solution, which deplete the Intracellular Ca2+ Store, the ATP-induced Cai rise was greatly reduced. 6. Our results suggest that in single cells from rat portal vein, ATP releases Ca2+ from Intracellular Stores without involving InsP3, but via a Ca2+ release mechanism activated by Ca2+ influx through ATP-gated channels.

  • ca2 and sr2 entry induced ca2 release from the Intracellular ca2 Store in smooth muscle cells of rat portal vein
    The Journal of Physiology, 1993
    Co-Authors: Guillaume Gregoire, Gervaise Loirand, Pierre Pacaud
    Abstract:

    1. Changes in cytosolic free Ca2+ concentration ([Ca2+]i) induced by membrane depolarizations were investigated using indo-1 microspectrofluorimetry in single patch-clamped smooth muscle cells of rat portal vein at room temperature (20-21 degrees C) and in the presence of 2 mM Ca2+. 2. During a 1 s depolarization from -50 to -30 mV [Ca2+]i rose, but, although the Ca2+ current was terminated by repolarization to -50 mV, [Ca2+]i continued to increase in a regenerative manner. The delay between the end of the voltage step and the peak of the [Ca2+]i rise was reduced by increasing the depolarization. 3. When a second identical depolarization was rapidly applied (8-13s) after the first one, it induced an identical Ca2+ current but a smaller increase in [Ca2+]i which started to decay upon repolarization. 4. A low concentration of caffeine (0.05 mM), applied to cells showing a small depolarization-induced [Ca2+]i transient which reached a peak at the end of the voltage step, produced an increase in amplitude and in duration of the [Ca2+]i rise without changing the amplitude of the depolarization-induced Ca2+ current. 5. The depolarization-induced [Ca2+]i rise was shortened and reduced in amplitude after noradrenaline- (NA 10 microM) or caffeine- (5 mM) induced release of Ca2+ Store and when the patch pipette solution contained ryanodine (100 microM). Under these conditions, the depolarization-induced [Ca2+]i transient was maximal at the end of the voltage step and declined immediately when the membrane was repolarized at -50 mV. 6. Experiments were done by replacing extracellular Ca2+ by Sr2+. Depolarization-induced Sr2+ entry through voltage-dependent Ca2+ channels could evoke an increase in indo-1 fluorescence which occurred after the termination of the voltage step. This delayed component of fluorescence increase displayed properties similar to those of the regenerative [Ca2+]i rise recorded in the Ca(2+)-containing solution. 7. The inefficiency of the second of two successive depolarizations to produce the delayed component of [Ca2+]i rise was not due to the emptiness of the Intracellular Ca2+ Store since, under these conditions, caffeine was still able to induce a Ca2+ release. 8. It is concluded that depolarization-evoked Ca2+ or Sr2+ entry through voltage-dependent Ca2+ channels induced the release of Ca2+ from an Intracellular Store, which could occur in a regenerative manner, independent of the termination of the triggering current.

Takuo Fujita - One of the best experts on this subject based on the ideXlab platform.

  • rapid ca2 refilling system of Intracellular Store s in human vascular endothelial cells
    Biochemical and Biophysical Research Communications, 1990
    Co-Authors: Shoichiro Takata, Masaaki Fukase, Yasuyuki Takagi, Osamu Tokunaga, Takuo Fujita
    Abstract:

    Using a fura-2 method, cytosolic Ca2+ concentration ([Ca2+]i) was measured in endothelial cell monolayers from human umbilical vein. In the presence of 1.5 mM Ca2+, bradykinin (BK) induced a rapid (within 15 sec) and dose-dependent (10−8–10−6 M) increase in [Ca2+]i, consisting of an initial peak and a subsequent sustained phase. The pretreatment with 3 mM EGTA for 1 min caused a significant reduction in [Ca2+]i levels both of the basal (p<0.05) and BK-stimulated initial peak (p<0.001). However, the BK-stimulated initial peak was retained in magnitude for at least 5 min under the treatment with EGTA. In contrast, the sustained phase was completely abolished by EGTA treatment. The BK-stimulated Ca2+ transient, once having been completely inhibited by ionomycin (10−6 M) in the presence of EGTA, was rapidly (within 2 min) recovered to the untreated level by replacing it with fresh medium containing 1.5 mM Ca2+. The present results indicated that BK mobilized Ca2+ from both Intracellular and extracellular space(s) and suggest the presence of an extracellular Ca2+-dependent rapid refilling system of Intracellular Ca2+ Store(s) in human vascular endothelial cells.

  • Rapid Ca2+ refilling system of Intracellular Store(s) in human vascular endothelial cells
    Biochemical and Biophysical Research Communications, 1990
    Co-Authors: Shoichiro Takata, Masaaki Fukase, Yasuyuki Takagi, Osamu Tokunaga, Takuo Fujita
    Abstract:

    Using a fura-2 method, cytosolic Ca2+ concentration ([Ca2+]i) was measured in endothelial cell monolayers from human umbilical vein. In the presence of 1.5 mM Ca2+, bradykinin (BK) induced a rapid (within 15 sec) and dose-dependent (10−8–10−6 M) increase in [Ca2+]i, consisting of an initial peak and a subsequent sustained phase. The pretreatment with 3 mM EGTA for 1 min caused a significant reduction in [Ca2+]i levels both of the basal (p