Effect of ATP on intracellular pH in pancreatic ducts involves P2X7 receptors.

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Effect of ATP on intracellular pH in pancreatic ducts involves P2X7 receptors. / Henriksen, Katerine L; Novak, Ivana.

In: Cellular Physiology and Biochemistry, Vol. 13, No. 2, 2003, p. 93-102.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Henriksen, KL & Novak, I 2003, 'Effect of ATP on intracellular pH in pancreatic ducts involves P2X7 receptors.', Cellular Physiology and Biochemistry, vol. 13, no. 2, pp. 93-102. https://doi.org/10.1159/000070253

APA

Henriksen, K. L., & Novak, I. (2003). Effect of ATP on intracellular pH in pancreatic ducts involves P2X7 receptors. Cellular Physiology and Biochemistry, 13(2), 93-102. https://doi.org/10.1159/000070253

Vancouver

Henriksen KL, Novak I. Effect of ATP on intracellular pH in pancreatic ducts involves P2X7 receptors. Cellular Physiology and Biochemistry. 2003;13(2):93-102. https://doi.org/10.1159/000070253

Author

Henriksen, Katerine L ; Novak, Ivana. / Effect of ATP on intracellular pH in pancreatic ducts involves P2X7 receptors. In: Cellular Physiology and Biochemistry. 2003 ; Vol. 13, No. 2. pp. 93-102.

Bibtex

@article{260564b0b18411ddb04f000ea68e967b,
title = "Effect of ATP on intracellular pH in pancreatic ducts involves P2X7 receptors.",
abstract = "Pancreatic acini release ATP, which can stimulate HCO3--secreting ducts that express purinergic receptors from both P2X and P2Y families. The aim of this study was to investigate whether extracellular ATP affects HCO3- or H+ transport across the plasma membrane of intralobular ducts, and determine which P2 receptors might be involved. Ducts were obtained from rat pancreas, and the pH sensitive fluorophore BCECF was used to measure pHi and recovery rates from cellular acidosis induced by ammonium pre-pulses. In order to reveal Na+/H+ exchange, Cl-/HCO3- exchange or a Na+-HCO3- cotransport, experiments were performed in solutions with or without bicarbonate buffers (+BIC or -BIC), with amiloride derivative EIPA, or with low extracellular Cl- concentrations. Although these transporters contributed to pHi recovery from acidosis, ATP had no effect. Nevertheless, ATP induced a small and reversible decrease in pHi by 0.07+/-0.02 pH-units and BzATP decreased pHi by 0.29+/-0.07 pH-units in -BIC (n=10, 11). These effects were abolished by Brilliant Blue and in Ca2+-free solutions. Our study shows that the pHi effect of ATP is mediated by P2X7 receptors. However, ATP does not affect H+/HCO3- transporters unmasked by cellular acidosis. Presumably, ATP alone does not stimulate HCO3- secretion in pancreatic ducts.",
author = "Henriksen, {Katerine L} and Ivana Novak",
note = "Keywords: Adenosine Triphosphate; Animals; Biological Transport; Carbonates; Female; Hydrogen-Ion Concentration; Intracellular Fluid; Pancreatic Ducts; Rats; Rats, Wistar; Receptors, Purinergic P2",
year = "2003",
doi = "10.1159/000070253",
language = "English",
volume = "13",
pages = "93--102",
journal = "Cellular Physiology and Biochemistry",
issn = "1015-8987",
publisher = "S Karger AG",
number = "2",

}

RIS

TY - JOUR

T1 - Effect of ATP on intracellular pH in pancreatic ducts involves P2X7 receptors.

AU - Henriksen, Katerine L

AU - Novak, Ivana

N1 - Keywords: Adenosine Triphosphate; Animals; Biological Transport; Carbonates; Female; Hydrogen-Ion Concentration; Intracellular Fluid; Pancreatic Ducts; Rats; Rats, Wistar; Receptors, Purinergic P2

PY - 2003

Y1 - 2003

N2 - Pancreatic acini release ATP, which can stimulate HCO3--secreting ducts that express purinergic receptors from both P2X and P2Y families. The aim of this study was to investigate whether extracellular ATP affects HCO3- or H+ transport across the plasma membrane of intralobular ducts, and determine which P2 receptors might be involved. Ducts were obtained from rat pancreas, and the pH sensitive fluorophore BCECF was used to measure pHi and recovery rates from cellular acidosis induced by ammonium pre-pulses. In order to reveal Na+/H+ exchange, Cl-/HCO3- exchange or a Na+-HCO3- cotransport, experiments were performed in solutions with or without bicarbonate buffers (+BIC or -BIC), with amiloride derivative EIPA, or with low extracellular Cl- concentrations. Although these transporters contributed to pHi recovery from acidosis, ATP had no effect. Nevertheless, ATP induced a small and reversible decrease in pHi by 0.07+/-0.02 pH-units and BzATP decreased pHi by 0.29+/-0.07 pH-units in -BIC (n=10, 11). These effects were abolished by Brilliant Blue and in Ca2+-free solutions. Our study shows that the pHi effect of ATP is mediated by P2X7 receptors. However, ATP does not affect H+/HCO3- transporters unmasked by cellular acidosis. Presumably, ATP alone does not stimulate HCO3- secretion in pancreatic ducts.

AB - Pancreatic acini release ATP, which can stimulate HCO3--secreting ducts that express purinergic receptors from both P2X and P2Y families. The aim of this study was to investigate whether extracellular ATP affects HCO3- or H+ transport across the plasma membrane of intralobular ducts, and determine which P2 receptors might be involved. Ducts were obtained from rat pancreas, and the pH sensitive fluorophore BCECF was used to measure pHi and recovery rates from cellular acidosis induced by ammonium pre-pulses. In order to reveal Na+/H+ exchange, Cl-/HCO3- exchange or a Na+-HCO3- cotransport, experiments were performed in solutions with or without bicarbonate buffers (+BIC or -BIC), with amiloride derivative EIPA, or with low extracellular Cl- concentrations. Although these transporters contributed to pHi recovery from acidosis, ATP had no effect. Nevertheless, ATP induced a small and reversible decrease in pHi by 0.07+/-0.02 pH-units and BzATP decreased pHi by 0.29+/-0.07 pH-units in -BIC (n=10, 11). These effects were abolished by Brilliant Blue and in Ca2+-free solutions. Our study shows that the pHi effect of ATP is mediated by P2X7 receptors. However, ATP does not affect H+/HCO3- transporters unmasked by cellular acidosis. Presumably, ATP alone does not stimulate HCO3- secretion in pancreatic ducts.

U2 - 10.1159/000070253

DO - 10.1159/000070253

M3 - Journal article

C2 - 12649594

VL - 13

SP - 93

EP - 102

JO - Cellular Physiology and Biochemistry

JF - Cellular Physiology and Biochemistry

SN - 1015-8987

IS - 2

ER -

ID: 8569829