Nicotine-evoked cytosolic Ca2+ increase and cell depolarization in capillary endothelial cells of the bovine adrenal medulla

Vinet, Raúl; Cortés, Magdalena P.; Luxoro, Mario; Delpiano, M. A.

doi:10.4067/s0716-97602009000100012

Cited by 7 publications

(9 citation statements)

References 28 publications

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“…The following features suggest that the voltage-gated currents measured in BAMCECs belong to the L-and T-type described in endocrine secretory cells: their kinetic and gating properties, currentvoltage relationships, sensitivity to BAY K 8644, nifedipine, and amiloride, and their different selectivity for Ba 2+ and Ca 2+ [156] . The T-type transient current displayed a conductance of 8 pS and may contribute to depolarisation-induced Ca 2+ influx [155,166] , while the L-type large current manifests a single-channel conductance of 20 pS and is affected by dihydropyridines [154] . Besides T-and L-type VOC, BAMCECs express a voltage-dependent Ca 2+ channel (termed SB) that shows a single-channel conductance of 2.8 pS in 100 mmol/L Ba 2+ and is sensitive to BAY K 8644, but not nicardipine [154] .…”

Section: Voltage-gated Camentioning

confidence: 99%

See 1 more Smart Citation

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Moccia

Berra‐Romani²,

Tanzi³

2012

WJBC

110

192

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A monolayer of endothelial cells (ECs) lines the lumen of blood vessels and forms a multifunctional transducing organ that mediates a plethora of cardiovascular processes. The activation of ECs from as state of quiescence is, therefore, regarded among the early events leading to the onset and progression of potentially lethal diseases, such as hypertension, myocardial infarction, brain stroke, and tumor. Intracellular Ca 2+ signals have long been know to play a central role in the complex network of signaling pathways regulating the endothelial functions. Notably, recent work has outlined how any change in the pattern of expression of endothelial channels, transporters and pumps involved in the modulation of intracellular Ca 2+ levels may dramatically affect whole body homeostasis. Vascular ECs may react to both mechanical and chemical stimuli by generating a variety of intracellular Ca 2+ signals, ranging from brief, localized Ca 2+ pulses to prolonged Ca 2+ oscillations engulfing the whole cytoplasm. The well-defined spatiotemporal profile of the subcellular Ca 2+ signals elicited in ECs by specific extracellular inputs depends on the interaction between Ca 2+ releasing channels, which are located both on the plasma membrane and in a number of intracellular organelles, and Ca 2+ removing systems. The present article aims to summarize both the past and recent literature in the field to provide a clear-cut picture of our current knowledge on the molecular nature and the role played by the components of the Ca 2+ machinery in vascular ECs under both physiological and pathological conditions.

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Section: Voltage-gated Camentioning

confidence: 99%

“…Activation of the latter does not elicit any detectable Ca 2+ influx in vascular endothelium [174] , while the former triggers a proangiogenic Ca 2+ entry that might be exploited to enhance tissue revascularization [173,175] . Moreover, nAChRs-mediated membrane depolarization induces VOCs-dependent Ca 2+ inrush in BAMCECs [166] .…”

Section: Rocs In Ecsmentioning

confidence: 99%

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Moccia

Berra‐Romani²,

Tanzi³

2012

WJBC

110

192

View full text Add to dashboard Cite

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“…This supports the assumption that thapsigargin and bradykinin operate on separated SERs in the intracellular space and that they may exhibit different thapsigargin isoforms. BAMCECs are complex cell units with different receptors and ion channels (Delpiano and Altura, 1996;Vinet and Vargas, 1999;Delpiano, 2000), as well as a 1 -adrenergic (Vinet et al, 2000) and nicotinicreceptors (Vinet et al, 2009). In this case, the previous [Ca 2þ ] i increase induced by bradykinin will be abolished by caffeine, that has depleted both SER stores ( Figure 7A).…”

Section: Discussionmentioning

confidence: 99%

“…However, in cultured porcine aortic ECs (Az-ma et al, 1995) Co 2þ , as well as Ni 2þ or zero external Ca 2þ , in pulmonary artery ECs (Cannell et al, 1989;Cannell and Sage, 1989), depressed the biphasic [Ca 2þ ] i increase induced by bradykinin. This assertion is because the same BAMCECs respond with a biphasic [Ca 2þ ] i increase when stimulated by catecholamine or nicotine (Vinet et al, 2000;2009). This assertion is because the same BAMCECs respond with a biphasic [Ca 2þ ] i increase when stimulated by catecholamine or nicotine (Vinet et al, 2000;2009).…”

Section: Discussionmentioning

confidence: 99%

Bradykinin and histamine‐induced cytosolic calcium increase in capillary endothelial cells of bovine adrenal medulla

Vinet

Cortés

Álvarez

et al. 2014

Cell Biology International

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We have assessed the effect of bradykinin and histamine on the cytosolic free calcium concentration ([Ca(2+)]i ) of bovine adrenal medulla capillary endothelial cells (BAMCECs). To measure [Ca(2+)]i changes in BAMCECs the intracellular fluorescent probe, fluo-3 AM, was used. Bradykinin (3 µM) produced a transient monophasic increase in [Ca(2+)]i , which was depressed by B1650 (0.1 µM), a B2-bradykinin receptor antagonist (D-Arg-[Hyp(3), Thi(5,8) , D-Phe(7)]-Bradykinin). Similarly, increase in [Ca(2+)]i induced by histamine was also depressed by tripolidine (0.1 µM), an H1-histamine receptor antagonist. [Ca(2+)]i increase induced by both agonists was unaffected in the absence of extracellular Ca(2+) or presence of antagonists of voltage operated Ca(2+) channels (VOCCs). Thapsigargin (1 µM) did not abolish the increase of [Ca(2+)]i produced by bradykinin, but abolished that of histamine. In contrast, caffeine (100 µM), abolished the [Ca(2+)]i response induced by bradykinin (3 µM), but did not affect the [Ca(2+)]i increase induced by histamine (100 µM). The results indicate the presence of B2 bradykinin- and H1 histamine-receptors in BAMCECs. Liberation of Ca(2+) induced by both agonists occurs through 2 different intracellular mechanisms. While bradykinin activates a sarco(endo) plasmic reticulum (SER) containing a SER Ca(2+) -ATPase (SERCA) thapsigargin-insensitive, histamine activates a SER containing a SERCA thapsigargin-sensitive. We suggest that the increase in [Ca(2+)]i induced by bradykinin and histamine could be of physiological relevance, modulating adrenal gland microcirculation.

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“…[Ca 2+ ] i was measured in a cell group (10–14 cells) using the fluorescent indicator Fluo‐3 AM (Vinet et al, ). HUVEC attached to coverslips were incubated with Fluo‐3 AM (7 µmol/L) and 0.094% pluronic acid in Locke's solution for 20 min at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of ATP‐induced calcium influx by homocysteine in human umbilical vein endothelial cells

Cortés

Becerra

Vinet

et al. 2013

Cell Biology International

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Mechanisms involved in the association between hyperhomocysteinemia and vascular occlusive diseases remain unclear. Homocysteine (Hcy) may disturb calcium (Ca(2+) ) cytosolic regulation in endothelial cells, a process that can directly affect the synthesis of vasoactive substances, such as nitric oxide (NO). We have investigated the effect of acute and chronic incubation with high concentrations of Hcy (100 and 500 μmol/L) on the changes in the intracellular Ca(2+) concentration ([Ca(2+) ]i ) induced by ATP, using primary cultures of human umbilical vein endothelial cells (HUVEC). The changes in [Ca(2+) ]i , expressed as ΔFt /Fb , were measured using the microspectrofluorimetric technique with Fluo-3 as Ca(2+) indicator. HUVEC acutely exposed to Hcy did not produce significant effects on any of the parameters studied. However, chronic exposition (24 h) caused a significant decrease in the speed of store-mediated Ca(2+) entry, expressed as (ΔFt /Fb )/t (s(-1) ). Exposure of HUVEC to 100 and 500 µmol/L Hcy gave significantly lower values (0.019 ± 0.002 s(-1) , n = 5 and 0.021 ± 0.004 s(-1) , n = 6, respectively) compared to the controls (0.046 ± 0.004 s(-1) , n = 8, P < 0.003). This was detected only when the sustained phase of the ATP-induced [Ca(+2) ]i increase was isolated. These results demonstrate that high concentrations of Hcy can affect the mechanisms involved in [Ca(2+) ]i regulation of HUVEC, and that alteration occurs specifically in the sustained phase, which has been directly associated with NO synthesis.

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Nicotine-evoked cytosolic Ca2+ increase and cell depolarization in capillary endothelial cells of the bovine adrenal medulla

Cited by 7 publications

References 28 publications

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Bradykinin and histamine‐induced cytosolic calcium increase in capillary endothelial cells of bovine adrenal medulla

Inhibition of ATP‐induced calcium influx by homocysteine in human umbilical vein endothelial cells

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Nicotine-evoked cytosolic Ca2+ increase and cell depolarization in capillary endothelial cells of the bovine adrenal medulla

Cited by 7 publications

References 28 publications

Update on vascular endothelial Ca2+signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca2+signalling: A tale of ion channels, pumps and transporters

Bradykinin and histamine‐induced cytosolic calcium increase in capillary endothelial cells of bovine adrenal medulla

Inhibition of ATP‐induced calcium influx by homocysteine in human umbilical vein endothelial cells

Contact Info

Product

Resources

About

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters