The Effects of 2-Aminoethoxydiphenyl Borate, a Novel Inositol 1,4,5-Trisphosphate Receptor Modulator on Myometrial Contractions

Ascher-Landsberg, Jessica; Saunders, Trevania; Elovitz, Michal A.; Phillippe, Mark

doi:10.1006/bbrc.1999.1602

Cited by 66 publications

(55 citation statements)

References 12 publications

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“…Electrophysiological studies have shown that 2-APB acts at the external surface of the cell rather than intracellularly (16,21,40,41). Although 2-APB may act on a target upstream from SOCs (11,14,15,42), it has been shown to be rather selective for SOCs because it has no effect on voltagedependent (18,43,44), S-nitrosylation-activated (45), diacylglycerol-activated (11,46), or arachidonic acid-gated Ca 2ϩ channels (18,47). To determine whether cytochrome P-450 metabolites are involved in the activation of SOCs in corneal endothelial cells, we first examined whether enhancement of CCE by the cytochrome P-450 inducer BN could be inhibited by the CCE blocker 2-APB.…”

Section: Methodsmentioning

confidence: 99%

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Calcium Influx Factor from Cytochrome P-450 Metabolism and Secretion-like Coupling Mechanisms for Capacitative Calcium Entry in Corneal Endothelial Cells

Xie

Zhang

Zhai

et al. 2002

Journal of Biological Chemistry

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Section: Methodsmentioning

confidence: 99%

“…In numerous cells, application of the phosphatase inhibitor CalyA induces condensation of the actin cytoskeleton at the PM (15,17,44,45). CalyA enhances association of ezrin, radixin, and moesin proteins, powerful mediators of actin cross-linking, with the PM (54,55).…”

Section: A Secretion-like Coupling Mechanism In Corneal Endothelialmentioning

confidence: 99%

Calcium Influx Factor from Cytochrome P-450 Metabolism and Secretion-like Coupling Mechanisms for Capacitative Calcium Entry in Corneal Endothelial Cells

Xie

Zhang

Zhai

et al. 2002

Journal of Biological Chemistry

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“…It did not affect caffeine-activated Ca 2+ release from striated muscle vesicles [9] or toad sinus venosus [14]. Furthermore, in smooth muscle, 2-APB inhibited contractile responses to InsP 3 -generating stimuli, but not those triggered by KCl-induced depolarisation [9,15,16] suggesting that there was no effect on voltage-operated Ca 2+ entry or the contractile machinery. Even though 2-APB may have no effect on RyRs or voltage-operated Ca 2+ channels, it is clearly not entirely specific for InsP 3 Rs [10] and in some cell types inhibition of InsP 3 -induced Ca 2+ release is not observed at all (e.g.…”

Section: Introductionmentioning

confidence: 94%

2-Aminoethoxydiphenyl borate (2-APB) antagonises inositol 1,4,5-trisphosphate-induced calcium release, inhibits calcium pumps and has a use-dependent and slowly reversible action on store-operated calcium entry channels

et al. 2003

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“…Furthermore, to determine whether an IP 3 -dependent mechanism was involved in intracellular Ca 2ϩ release, the effect of AII was tested in the presence of 2-aminoethoxydiphenyl borate (2-APB, 200 mol/L, Calbiochem), a specific IP 3 receptor blocker. 15 To assess the contribution of the Na-Ca exchange mechanism, AII experiments were performed under extracellular Na ϩ -free conditions. Na ϩ -free buffer was prepared by either substituting 124 mmol/L Na ϩ with equimolar N-methyl-D-glucamine (NMG) or with LiCl (Sigma-Aldrich).…”

Section: Pharmacological Interventionsmentioning

confidence: 99%

Modulation of Angiotensin II Responses in Sympathetic Neurons by Cytosolic Calcium

et al. 2003

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Abstract-Both stimulatory and suppressive responses of the sympathetic nervous system to angiotensin II (AII) Key Words: sympathetic nervous system Ⅲ angiotensin II Ⅲ calcium Ⅲ calcium channel blockers Ⅲ norepinephrine Ⅲ inositol T he renin-angiotensin and sympathetic nervous systems are homeostatically interconnected by a complex series of mutually reinforcing and mutually inhibiting interactions. In general, each of these systems tends to reinforce the pressor effects of the other as the two systems act to defend arterial pressure. Sympathetic stimulation is a major controller of juxtaglomerular cell renin release through the actions of catecholamines on juxtaglomerular cell ␤ 1 receptors. 1 The angiotensin II (AII) subsequently generated in the bloodstream can exert positive feedback on sympathetic nervous activity by several complex mechanisms, including direct stimulatory actions of AII on central and peripheral sympathetic neuronal activity and catecholamine release. [1][2][3] In addition to its stimulatory effects, AII can also suppress sympathetic neuronal activity in vivo. In animals and humans, complex reflex inhibition occurs when increases in arterial pressure stimulate arterial baroreflexes to cause reflex suppression of sympathetic nervous outflow. A more confusing picture emerges in whole-animal experiments designed to isolate the contributions of the peripheral sympathetic nervous system: AII infusion can facilitate, 4 suppress, 5 or have no effect 6 on norepinephrine release from postganglionic sympathetic neurons. In humans, a similar pattern of sympathetic neural responses has been reported, with some studies showing increased norepinephrine spillover 3 and others showing no response 7 or decreased norepinephrine release 3,7,8 in response to AII. In other excitable cell types such as cardiomyocytes or vascular smooth muscle cells, a paradoxical response has also been reported. AII treatment was shown to increase cytosolic calcium ([Ca 2ϩ ]i) by stimulation of IP 3 -dependent pathways 9,10 and was also reported to decrease [Ca 2ϩ ]i through enhanced calcium efflux. 11,12 The current studies were undertaken to examine the effects of AII on neuronal [Ca 2ϩ ]i and to investigate whether alterations in [Ca 2ϩ ]i play a role in the apparent "bidirectional" excitatory and suppressive responses to AII seen in sympathetic neurons studied in vivo. Using isolated primary sympathetic neurons from rats, we first related neuronal responses to the dose of AII and to the baseline [Ca 2ϩ ]i. To confirm that the same neuron is capable of both stimulatory and suppressive responses to AII, cells with spontaneously low [Ca 2ϩ ]i were exposed to a Ca 2ϩ ionophore and cells with spontaneously high [Ca 2ϩ ]i were exposed to nifedipine. We used losartan to investigate the role of the AT 1 receptors and confirmed IP 3 pathway dependency with an IP 3 receptor blocker and by prior

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The Effects of 2-Aminoethoxydiphenyl Borate, a Novel Inositol 1,4,5-Trisphosphate Receptor Modulator on Myometrial Contractions

Cited by 66 publications

References 12 publications

Calcium Influx Factor from Cytochrome P-450 Metabolism and Secretion-like Coupling Mechanisms for Capacitative Calcium Entry in Corneal Endothelial Cells

Calcium Influx Factor from Cytochrome P-450 Metabolism and Secretion-like Coupling Mechanisms for Capacitative Calcium Entry in Corneal Endothelial Cells

2-Aminoethoxydiphenyl borate (2-APB) antagonises inositol 1,4,5-trisphosphate-induced calcium release, inhibits calcium pumps and has a use-dependent and slowly reversible action on store-operated calcium entry channels

Modulation of Angiotensin II Responses in Sympathetic Neurons by Cytosolic Calcium

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