5-Hydroxytryptamine induces transient Ca2+ influx through Ni2+-insensitive Ca2+ channels in rat vascular smooth muscle cells

Hirafuji, Masahiko; Kawahara, Fumito; Ebihara, Takashi; Nezu, Akihiro; Tanimura, Akihiko; Minami, Masaru

doi:10.1016/s0014-2999(99)00532-4

Cited by 8 publications

(3 citation statements)

References 30 publications

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“…Note that the duration of the first transient and, consequently, the interval between the first and the second spike are significantly lower at 7.5 ng/ml. low concentrations (Manabe et al, 1995;Hirafuji et al, 1999;Usachev and Thayer, 1999;Jung et al, 2000). Indeed, 100 mM Ni 2þ (n ¼ 14; Fig.…”

Section: Dose-dependence Of the Response To Egfmentioning

confidence: 90%

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: 90%

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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“…[Ca 2+ ]i was measured as described previously [16,17]. Cells seeded and grown on cover glasses (8 × 16 mm) were loaded with 5 μ m fura‐2 acetoxymethyl ester (fura‐2/AM) for 45 min at 37°C in Hank's balanced salt solution containing 0.1% bovine serum albumin and 10 mM HEPES (HBSS; pH 7.4).…”

Section: Methodsmentioning

confidence: 99%

Sphingosine 1-phosphate increases an intracellular Ca2+ concentration via S1P3 receptor in cultured vascular smooth muscle cells

Fujii

Machida

Iizuka

et al. 2014

Journal of Pharmacy and Pharmacology

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“…5-Hydroxytryptamine is known to have a direct effect on outward K + and inward Ca 2+ currents in various smooth muscle tissues. In vascular smooth muscle cells, 5-HT increases the intracellular calcium concentration ([Ca 2+ ] i ) by activating L-type voltage-dependent Ca 2+ channels, [17][18][19] as well as by mobilizing Ca 2+ from intracellular stores. 20 In the gastrointestinal tract, 5-HT induces contraction of rat isolated stomach fundus by activating Ca 2+ -sensitive Cl -(Cl Ca ) channels, leading to calcium entry via Ca 2+ channels.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms Mediating Serotonin‐induced Contraction of Colonic Myocytes

Chen

et al. 2006

Clin Exp Pharma Physio

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1. 5-Hydroxytryptamine (5-HT) has an important role in the pathogenesis of irritable bowel syndrome. To investigate the effects of 5-HT on the contractile activity of myocytes of the guinea-pig proximal colon, cell imaging before and after contraction was undertaken and images were analysed using image-analysis software. Ion currents and membrane potentials were measured. Cytoplasmic free Ca(2+) was recorded using a confocal microscope following loading of the cells with the fluorescent probe Fura-2AM. 2. 5-Hydroxytryptamine reduced cell length in a dose-dependent manner (EC(50) = 0.189 micromol/L). Under current clamp, 10 micromol/L 5-HT reduced action potential amplitude (measured as peak height) and decreased action potential duration, as well as depolarizing the resting potential from -68.4 +/- 3.6 to -22.96 +/- 4.65 mV. Iberiotoxin (1 micromol/L) blocked the effects of 5-HT in reducing the time to repolarization (T(90)) and nicardipine (5 micromol/L) blocked the effects of 5-HT in reducing action potential amplitude. 3. In the whole-cell mode, 5-HT enhanced L-type Ca(2+) currents, large conductance K(+) channel (BK(Ca)) currents and spontaneous transient outward currents (STOC). In addition, 5-HT increased intracellular Ca(2+) levels. Ondansetron (10 micromol/L) blocked the effects of 5-HT in enhancing L-type Ca(2+) currents, BK(Ca) currents and STOC. 4. In conclusion, 5-HT induces contraction of colonic myocytes, mostly as a result of Ca(2+) release from the sarcoplasmic reticulum (SR) following activation of 5-HT(3) receptors and the inositol 1,4,5-trisphosphate pathway. In addition, the effect of 5-HT in decreasing action potential amplitude is mediated by the release of Ca(2+) from the SR, as well as by enhanced L-type Ca(2+) current. 5-Hydroxytryptamine decreased action potential duration by enhancing BK(Ca) current.

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5-Hydroxytryptamine induces transient Ca2+ influx through Ni2+-insensitive Ca2+ channels in rat vascular smooth muscle cells

Cited by 8 publications

References 30 publications

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

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

Sphingosine 1-phosphate increases an intracellular Ca2+ concentration via S1P3 receptor in cultured vascular smooth muscle cells

Mechanisms Mediating Serotonin‐induced Contraction of Colonic Myocytes

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5-Hydroxytryptamine induces transient Ca2+ influx through Ni2+-insensitive Ca2+ channels in rat vascular smooth muscle cells

Cited by 8 publications

References 30 publications

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

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

Sphingosine 1-phosphate increases an intracellular Ca2+ concentration via S1P3 receptor in cultured vascular smooth muscle cells

Mechanisms Mediating Serotonin‐induced Contraction of Colonic Myocytes

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

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