Ca2+ release and activation of K+ and Cl- currents by extracellular ATP in distal nephron epithelial cells

Nilius, Bernd; Sehrer, J; Heinke, Stephan; Droogmans, Guillaume

doi:10.1152/ajpcell.1995.269.2.c376

Cited by 32 publications

(30 citation statements)

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“…However, it should be noted that a 10-min incubation in a calcium-free medium could also have depleted the Ca2 , stores, thus ren dering a final interpretation of these experiments difficult. In order to investigate this, we observed the effects o f ATP which as recently been shown to increase Ca2 , by releasing Ca2', [30]. As shown in figure 7.…”

Section: Origin O F the Hypo-osmotically-induced Ca2' / Increasementioning

confidence: 97%

Characterisation of Ca2+ Membrane Permeability of Renal A6 Cells upon Different Osmotic Conditions

Brochiero¹,

Ehrenfeld²

1997

Kidney Blood Press Res

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The nature of the calcium-transporting mechanisms involved in A6 cell calcium homeostasis under iso- and hypo-osmotic conditions was investigated using fura-2 (AM) as a cell calcium indicator. Under steady-state conditions, intracellular calcium (Ca²⁺_i) was increased by Bay K8644 or by gramicidin, an ionophore which depolarises A6 cell membranes. The Ca²⁺_i increase following calcium addition (to calcium-depleted cells) or membrane depolarisation was blocked by nifedipine but not by verapamil or ω-conotoxin, indicating that the membrane calcium permeability may be mediated by voltage-dependent and dihydropyridine-sensitive calcium channels. Ca²⁺_i could also be increased by a hypo-osmotic shock having a linear relationship with the osmolarity change. This osmotically induced Ca²⁺_i increase had an extracellular origin since it was absent when cells were suspended in a calcium-free medium and it was not affected by thapsigargin or TMB-8 application. In addition, it was inhibited by the calcium channel inhibitor, nifedipine. Furthermore, under hypo-osmotic conditions, an additional Ca²⁺_i increase, sensitive to nifedipine, was measured when cells were depolarised by gramicidin or K-gluconate addition. It is proposed that the hypo-osmotically induced cell calcium increase implies the activation of voltage-dependent and nifedipine-sensitive calcium channels, presenting the same pharmacological characteristics as those involved in cell calcium homeostasis under iso-osmotic conditions. The initial Ca²⁺_i increase was transient and stabilised to a value nevertheless higher than the iso-osmotic level; this secondary and incomplete regulatory phase did not occur in the presence of thapsigargin or TMB-8, thus providing evidence of intracellular calcium storage.

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Section: Origin O F the Hypo-osmotically-induced Ca2' / Increasementioning

confidence: 97%

Characterisation of Ca2+ Membrane Permeability of Renal A6 Cells upon Different Osmotic Conditions

Brochiero¹,

Ehrenfeld²

1997

Kidney Blood Press Res

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“…However, many of the studies of distal tubule cells have been carried out on cell lines such as A6 (derived from Xenopus kidney) and Madin-Darby canine kidney (MDCK) cell. ATP activates both Cl − and K + channels in distal nephron epithelial cells from the cell line A6 by a Ca 2+ -dependent mechanism [243,257,315], probably via P2Y 2 receptors [19, 250,251] and also in a rabbit distal convoluted tubule cell line [26]. The high-affinity Ca 2+ channel of the distal tubule luminal membrane is regulated by ATP, and ATP plays a crucial role in the integrity of the cytoskeleton, which is also involved in the control of Ca 2+ channels in this membrane [35,284].…”

Section: Distal Tubulesmentioning

confidence: 99%

Purinergic signalling in the kidney in health and disease

Burnstock

Evans

Bailey

2013

Purinergic Signalling

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The involvement of purinergic signalling in kidney physiology and pathophysiology is rapidly gaining recognition and this is a comprehensive review of early and recent publications in the field. Purinergic signalling involvement is described in several important intrarenal regulatory mechanisms, including tuboglomerular feedback, the autoregulatory response of the glomerular and extraglomerular microcirculation and the control of renin release. Furthermore, purinergic signalling influences water and electrolyte transport in all segments of the renal tubule. Reports about purine-and pyrimidine-mediated actions in diseases of the kidney, including polycystic kidney disease, nephritis, diabetes, hypertension and nephrotoxicant injury are covered and possible purinergic therapeutic strategies discussed.

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“…Activation of purinergic receptors by ATP induces the release of Ca 2+ from the ER. The key mechanism for ATP-mediated chloride secretion is intracellular Ca 2+ release, which in turn will active calcium-activated chloride channels (CaCC) [34]. In fact, a truncated form of PC1 has been shown to enhance ATP-stimulated chloride secretion in the mouse collecting duct cells [44].…”

Section: +mentioning

confidence: 99%

Polycystin-1, 2, and STIM1 Interact with IP3R to Modulate ER Ca2+ Release through the PI3K/Akt Pathway

Santoso

Cebotaru

Guggino

2011

Cell Physiol Biochem

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Dysregulation of Ca²⁺ signaling and homeostasis has been linked to the development of ADPKD through aberrant functioning of the polycystins. In this study, we investigated the role of the polycystins in modulating Ca²⁺ signaling. Expression of full-length PC1 in MDCK cells inhibited intracellular Ca²⁺ release in response to ATP when compared to control cells. This phenotype correlated with reduced interaction of endogenous PC2 and IP₃R in PC1-containing cells. We also found that endogenous STIM1 also interacted with the IP₃R, and this interaction was enhanced by PC1 expression. Increased interaction between STIM1 and IP₃R inhibited Ca²⁺ release. PC1 regulates intracellular Ca²⁺ release and the interaction of PC2-IP₃R-STIM1 through the PI3K/Akt signaling pathway. Inhibition of the PI3K/Akt pathway in PC1 containing cells restored intracellular Ca²⁺ release, increased the interaction between PC2 and IP₃R and disrupted the STIM1-IP₃R complex. Conversely, activation of the PI3K/Akt signaling pathway by HGF in control MDCK cells gave the reverse effects. It reduced the release of Ca²⁺ to levels comparable to the PC1 cells, inhibited the association PC2 and IP₃R, and increased the interaction between STIM and IP₃R. Overall, our studies provide a potential mechanism for the modulation of intracellular Ca²⁺ signaling by the polycystins.

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Ca2+ release and activation of K+ and Cl- currents by extracellular ATP in distal nephron epithelial cells

Cited by 32 publications

References 0 publications

Characterisation of Ca<sup>2+</sup> Membrane Permeability of Renal A6 Cells upon Different Osmotic Conditions

Characterisation of Ca<sup>2+</sup> Membrane Permeability of Renal A6 Cells upon Different Osmotic Conditions

Purinergic signalling in the kidney in health and disease

Polycystin-1, 2, and STIM1 Interact with IP<sub>3</sub>R to Modulate ER Ca<sup>2+</sup> Release through the PI3K/Akt Pathway

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