Caffeine‐evoked, calcium‐sensitive membrane currents in rabbit aortic endothelial cells

Rusko, J.; Slooten, Glen Van; Adams, David J.

doi:10.1111/j.1476-5381.1995.tb16330.x

Cited by 24 publications

(28 citation statements)

References 38 publications

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“…Note that an interval of about 10 min was kept between each BK application in order to avoid desensitization. However, in ECs endowed with ryanodine receptors, caffeine may also increase [Ca 2þ ] i by stimulating the Ca 2þ -induced Ca 2þ release (Rusko et al, 1995). However, the application of 2.5 mM or 10 mM caffeine to resting CMEC never increased [Ca 2þ ] i (n ¼ 16 and 10, respectively; not shown), thus suggesting it was without effect on ryanodine receptors.…”

Section: Dose-dependence Of the Response To Egfmentioning

confidence: 61%

Epidermal growth factor induces intracellular Ca²⁺ oscillations in microvascular endothelial cells

Moccia

Berra‐Romani

Tritto

et al. 2002

Journal Cellular Physiology

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An increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) may play a role in the proliferative effect of several growth factors. In this study, the changes in [Ca(2+)](i) elicited by epidermal growth factor (EGF) in rat cardiac microvascular endothelial cells (CMEC) have been investigated by using fura-2 conventional and confocal microscopy. A large heterogeneity in the latency and in the pattern of the Ca(2+) response was found at each dose of EGF (2.5-100 ng/ml), whereas some cells displayed a non-oscillatory behavior and others exhibited a variable number of Ca(2+) oscillations. On average, the fraction of responsive cells, the total number of oscillations and the duration of the Ca(2+) signal were higher at around 10 ng/ml EGF, while there was no dose-dependence in the lag time and in the amplitude of the [Ca(2+)](i) increase. EGF-induced Ca(2+) spikes were abolished by the tyrosine kinase inhibitor genistein, but not by its inactive analogue daidzein, and by the phospholipase C blocker NCDC. Only 1-2 transients could be elicited in Ca(2+)-free solution, while re-addition of extracellular Ca(2+) recovered the spiking activity. The oscillatory signal was prevented by the SERCA inhibitor thapsigargin and abolished by the calcium entry blockers Ni(2+) and La(3+). Moreover, EGF-induced Ca(2+) transients were abolished by the InsP(3) receptor blocker caffeine, while ryanodine was without effect. Confocal imaging microscopy showed that the Ca(2+) response to EGF was localized both in the cytoplasm and in the nucleus. We suggest that EGF-induced [Ca(2+)](i) increase may play a role in the proliferative action of EGF on endothelial cells.

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Section: Dose-dependence Of the Response To Egfmentioning

confidence: 61%

Epidermal growth factor induces intracellular Ca²⁺ oscillations in microvascular endothelial cells

Moccia

Berra‐Romani

Tritto

et al. 2002

Journal Cellular Physiology

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“…Similarly, endothelial cells from bovine and rabbit were also found to differ in their responses to caffeine. Caffeine did not produce a marked release of Ca 2ϩ from intracellular stores in bovine endothelial cells but was effective in rabbit aortic endothelial cells (70).…”

Section: Resultsmentioning

confidence: 79%

Ryanodine Receptor Type III (Ry3R) Identification In Mouse Parotid Acini

DiJulio

Watson

Pessah

et al. 1997

Journal of Biological Chemistry

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“…High-conductance "maxi" or big K Ca channels (BK Ca channels) have a conductance between 165 and 220 pS (8,66,83,114,146,148). They show Ca 2+ -and voltage-dependent activation and are blocked by TEA, charybdotoxin, d-tubocurarine (8,30,147), and by extracellular alkalinization (170).…”

Section: Potassium Channelsmentioning

confidence: 99%

Ion Channels in Vascular Endothelium

Nilius

Viana

Droogmans

1997

Annu. Rev. Physiol.

267

194

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The functional impact of ion channels in vascular endothelial cells (ECs) is still a matter of controversy. This review describes different types of ion channels in ECs and their role in electrogenesis, Ca2+ signaling, vessel permeability, cell-cell communication, mechano-sensor functions, and pH and volume regulation. One major function of ion channels in ECs is the control of Ca2+ influx either by a direct modulation of the Ca2+ influx pathway or by indirect modulation of K+ and Cl- channels, thereby clamping the membrane at a sufficiently negative potential to provide the necessary driving force for a sustained Ca2+ influx. We discuss various mechanisms of Ca2+ influx stimulation: those that activate nonselective, Ca(2+)-permeable cation channels or those that activate Ca(2+)-selective channels, exclusively or partially operated by the filling state of intracellular Ca2+ stores. We also describe the role of various Ca(2+)- and shear stress-activated K+ channels and different types of Cl- channels for the regulation of the membrane potential.

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Caffeine‐evoked, calcium‐sensitive membrane currents in rabbit aortic endothelial cells

Abstract: 1 Single cell photometry and whole-cell patch clamp recording were used to study caffeine-induced intracellular Ca2+ signals and membrane currents, respectively, in endothelial cells freshly dissociated from rabbit aorta.2 Caffeine (5 mM) evoked a transient increase in [Ca2+]

Cited by 24 publications

References 38 publications

Epidermal growth factor induces intracellular Ca²⁺ oscillations in microvascular endothelial cells

Epidermal growth factor induces intracellular Ca²⁺ oscillations in microvascular endothelial cells

Ryanodine Receptor Type III (Ry3R) Identification In Mouse Parotid Acini

Ion Channels in Vascular Endothelium

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Caffeine‐evoked, calcium‐sensitive membrane currents in rabbit aortic endothelial cells

Abstract: 1 Single cell photometry and whole-cell patch clamp recording were used to study caffeine-induced intracellular Ca2+ signals and membrane currents, respectively, in endothelial cells freshly dissociated from rabbit aorta.2 Caffeine (5 mM) evoked a transient increase in [Ca2+]

Cited by 24 publications

References 38 publications

Epidermal growth factor induces intracellular Ca2+ oscillations in microvascular endothelial cells

Epidermal growth factor induces intracellular Ca2+ oscillations in microvascular endothelial cells

Ryanodine Receptor Type III (Ry3R) Identification In Mouse Parotid Acini

Ion Channels in Vascular Endothelium

Contact Info

Product

Resources

About

Epidermal growth factor induces intracellular Ca²⁺ oscillations in microvascular endothelial cells

Epidermal growth factor induces intracellular Ca²⁺ oscillations in microvascular endothelial cells