Nitric oxide induces intracellular Ca<sup>2+</sup> mobilization and increases secretion of incorporated 5‐hydroxytryptamine in rat pancreatic β‐cells

Willmott, Nicholas J.; Galione, Antony; Smith, Paul A.

doi:10.1016/0014-5793(95)00848-4

Cited by 77 publications

(67 citation statements)

References 23 publications

(43 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It averaged 48% of the basal value and was more pronounced when the initial platelet [Ca2+]i level was low. A NO-mediated rise in the cytosolic [Ca2+] has also been described in other cell types including interstitial cells from canine colon (Publicover et al, 1993), rat pancreatic fl-cells (Willmott et al, 1995), intact sea urchin eggs (Willmott et al, 1996) and cultured nodose ganglion neurones from rabbits (Sato et al, 1996). In cells possessing I .…”

Section: Discussionmentioning

confidence: 82%

“…In cells possessing I . =24=zzi ryanodyne-sensitive Ca2+ channels, this Ca2+ rise can be partially due to the production of cyclic ADP-ribose, a Ca2+ mobilizing agent (Publicover et al, 1993;Willmott et al, 1995;. The presence of a ryanodine receptor mediated Ca21-induced Ca2+-release has not been established in platelets.…”

Section: Discussionmentioning

confidence: 99%

“…This inhibition could be caused by one or more independent mechanisms including an increase in platelet cyclic GMP levels. (Brune & Ullrich, 1991;Authi et al, 1993 and suppresses thromboxane generation in thrombin-stimulated human platelets (Sane et al, 1989 (Publicover et al, 1993;Willmott et al, 1995;Sato et al, 1996) questions the physiological significance of these NO effects on the NO-elicited Ca2+ increase. When the actual NO concentration available in the platelet suspension was controlled throughout the experiment by a NO-sensitive electrode and differential pulse amperometry, it was found to decrease from 5 to 2 gM within seconds after addition, and then to disappear slowly with an apparent half-life of approximately 400 s (unpublished data).…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Influence of authentic nitric oxide on basal cytosolic [Ca²⁺] and Ca²⁺ release from internal stores in human platelets

Sang

Lantoine

Devynck

1996

British J Pharmacology

View full text Add to dashboard Cite

Nitric oxide (NO) donors inhibit platelet function and Ca2+ mobilization evoked by different agonists. This led us to investigate the direct effects of authentic NO on basal cytosolic Ca2+ concentration ([Ca2+]i) and on Ca2+ mobilization induced by thrombin or by two inhibitors of intracellular Ca2+‐ATPases, thapsigargin and 2,5‐di‐(t‐butyl)‐l,4‐benzohydroquinone (t‐BuBHQ). Cytosolic Ca2+ concentration was evaluated with Fura‐2, in the absence of Ca2+ influx. Addition of 5 μm NO increased by 48% the basal cytosolic [Ca2+] of resting human platelets whereas a lower concentration (0.1 μm) did not induce significant modifications. This NO‐induced Ca2+ increase was inversely correlated with the basal level of cytosolic [Ca2+]. NO pretreatment for 30 to 120 s decreased by 42 to 57% the transient [Ca2+]i peak evoked by 0.10 u ml−1 thrombin and strongly attenuated the initial rate of [Ca2+]i rise induced by 1 μm thapsigargin or by 20 μm t‐BuBHQ. The two components of the thapsigargin response, the Ca2+ release due to inhibition of Ca2+ pumps and the thromboxane A2‐dependent self‐amplification mechanism, were inhibited by NO. The observation that a subsequent stimulation was still capable of eliciting Ca2+ release suggests the presence of NO‐insensitive Ca2+ stores. These findings indicate that nitric oxide can modulate basal cytosolic [Ca2+] in unstimulated human platelets and decrease the Ca2+ mobilization from NO‐sensitive internal stores evoked by stimulation of receptors or by Ca2+‐ATPase inhibitors. This underlines the important role of nitric oxide in the modulation of platelet Ca2+ handling.

show abstract

Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Influence of authentic nitric oxide on basal cytosolic [Ca²⁺] and Ca²⁺ release from internal stores in human platelets

Sang

Lantoine

Devynck

1996

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…There is also evidence suggesting that NO can facilitate neurotransmitter release in some experimental models (Prast and Philippu, 1992;Herring and Paterson, 2001). It should be recalled, however, that in addition to its action on HVA Ca 2ϩ channels, NO also enhances calcium release from intracellular stores (Willmott et al, 1995;Stoyanovsky et al, 1997), and the net result of these potentially contrasting effects may well depend on the experimental model used.…”

Section: Discussionmentioning

confidence: 99%

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

et al. 2002

View full text Add to dashboard Cite

Although data from our laboratory and others suggest that nitric oxide (NO) exerts an overall inhibitory action on high-voltageactivated Ca 2ϩ channels, conflicting observations have been reported regarding its effects on N-type channels. We performed whole-cell and cell-attached patch-clamp recordings in IMR32 cells to clarify the functional role of NO in the modulation of N channels of human neuronal cells. During depolarizing steps to ϩ10 mV from V h ϭ Ϫ90 mV, the NO donor, sodium nitroprusside (SNP; 200 M), reduced macroscopic N currents by 34% ( p Ͻ 0.01). The magnitude of inhibition was similar at all voltages tested (range, Ϫ40 to ϩ50 mV). No significant inhibition was observed when SNP was applied together with the NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (300 M), or after cell treatment with the guanylate cyclase inhibitor, 1H- channel open probability by 59% and increased both the mean shut time and the null sweep probability, but it had no significant effects on channel conductance, mean open time, or latency of first openings. These data suggest that NO inhibits N-channel gating through cGMP and PKG. The consequent decrease in Ca 2ϩ influx through these channels may affect different neuronal functions, including neurotransmitter release.

show abstract

“…2b,d,e), underscoring a specific effect for NO on intracellular Ca 2ϩ release in glia. It has previously been reported that NO-induced Ca 2ϩ mobilization is ryanodine receptor (RyR)-linked in several cell types (Publicover et al, 1993;Willmott et al, 1995a;Willmott et al, 1996c). To test for the involvement of a RyR-mediated Ca 2ϩ release mechanism, cells were preincubated with an antagonizing concentration of ryanodine before NO application.…”

Section: Nitric Oxide Induces Ca 2؉ Mobilization In Glial Cells Via Tmentioning

confidence: 99%

A Fundamental Role for the Nitric Oxide-G-Kinase Signaling Pathway in Mediating Intercellular Ca²⁺Waves in Glia

2000

Self Cite

View full text Add to dashboard Cite

In this study, we highlight a role for the nitric oxide-cGMPdependent protein kinase (NO-G-kinase) signaling pathway in glial intercellular Ca 2ϩ wave initiation and propagation. Addition of the NO donor molsidomine (100-500 M) or puffing aqueous NO onto primary glial cell cultures evoked an increase in [Ca 2ϩ ] i in individual cells and also local intercellular Ca 2ϩ waves, which persisted after removal of extracellular Ca 2ϩ . High concentrations of ryanodine (100-200 M) and antagonists of the NO-G-kinase signaling pathway essentially abrogated the NO-induced increase in [Ca 2ϩ ] i , indicating that NO mobilizes Ca 2ϩ from a ryanodine receptor-linked store, via the NO-G-kinase signaling pathway. Addition of 10 M nicardipine to cells resulted in a slowing of the molsidomine-induced rise in [Ca 2ϩ ] i , and inhibition of Mn 2ϩ quench of cytosolic fura-2 fluorescence mediated by a bolus application of 2 M aqueous NO to cells, indicating that NO also induces Ca 2ϩ influx in glia. Mechanical stress of individual glial cells resulted in an increase in intracellular NO in target and neighboring cells and intercellular Ca 2ϩ waves, which were NO, cGMP, and G-kinase dependent, because incubating cells with nitric oxide synthase, guanylate cyclase, and G-kinase inhibitors, or NO scavengers, reduced ⌬[Ca 2ϩ ] i and the rate of Ca 2ϩ wave propagation in these cultures. Results from this study suggest that NO-Gkinase signaling is coupled to Ca 2ϩ mobilization and influx in glial cells and that this pathway plays a fundamental role in the generation and propagation of intercellular Ca 2ϩ waves in glia. Key words: nitric oxide; glia; calcium waves; mobilization; influx; ryanodine receptors; nitric oxide synthase; DAF-2; phospholipase C; astrocytesIt is becoming increasingly apparent that intercellular Ca 2ϩ waves might be the result of combined contributions of intracellular and extracellular Ca 2ϩ signaling pathways in glial cells. One generally accepted mode of intercellular Ca 2ϩ wave propagation involves the diffusion of Ca 2ϩ mobilizing second messengers, including inositol-1,4,5-trisphosphate (IP 3 ) and Ca 2ϩ , across gap junctions (Nedergaard, 1994;Charles, 1998). Extracellular, gap junction-independent modes of Ca 2ϩ signaling, involving the release of a diffusible messengers, also appear to operate in this particular system however, with ATP release from cells and P 2 receptor-coupled elevation of [Ca 2ϩ ] i having recently been suggested as a likely candidate (Cotrina et al., 1998;Guthrie et al., 1999). There are however other species that may participate as extracellular messengers in glial intercellular Ca 2ϩ waves. There is increasing evidence that the highly diffusible messenger nitric oxide (NO) can induce Ca 2ϩ mobilization in several cell types (Publicover et al., 1993; Willmott et al., 1995a,b,c;Clementi et al., 1996) either via the cGMP-dependent protein kinase (G-kinase)-coupled activation of ADP-ribosyl cyclase, resulting in an increased synthesis of the potent Ca 2ϩ mobilizing agent cyclic ADP-rib...

show abstract

Nitric oxide induces intracellular Ca²⁺ mobilization and increases secretion of incorporated 5‐hydroxytryptamine in rat pancreatic β‐cells

Cited by 77 publications

References 23 publications

Influence of authentic nitric oxide on basal cytosolic [Ca²⁺] and Ca²⁺ release from internal stores in human platelets

Influence of authentic nitric oxide on basal cytosolic [Ca²⁺] and Ca²⁺ release from internal stores in human platelets

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

A Fundamental Role for the Nitric Oxide-G-Kinase Signaling Pathway in Mediating Intercellular Ca²⁺Waves in Glia

Contact Info

Product

Resources

About

Nitric oxide induces intracellular Ca2+ mobilization and increases secretion of incorporated 5‐hydroxytryptamine in rat pancreatic β‐cells

Cited by 77 publications

References 23 publications

Influence of authentic nitric oxide on basal cytosolic [Ca2+] and Ca2+ release from internal stores in human platelets

Influence of authentic nitric oxide on basal cytosolic [Ca2+] and Ca2+ release from internal stores in human platelets

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca2+Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

A Fundamental Role for the Nitric Oxide-G-Kinase Signaling Pathway in Mediating Intercellular Ca2+Waves in Glia

Contact Info

Product

Resources

About

Nitric oxide induces intracellular Ca²⁺ mobilization and increases secretion of incorporated 5‐hydroxytryptamine in rat pancreatic β‐cells

Influence of authentic nitric oxide on basal cytosolic [Ca²⁺] and Ca²⁺ release from internal stores in human platelets

Influence of authentic nitric oxide on basal cytosolic [Ca²⁺] and Ca²⁺ release from internal stores in human platelets

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

A Fundamental Role for the Nitric Oxide-G-Kinase Signaling Pathway in Mediating Intercellular Ca²⁺Waves in Glia