Modulation of calcium signals by intracellular pH in isolated rat pancreatic acinar cells

J Physiol. 1998 Jan 15;506 ( Pt 2)(Pt 2):415-30. doi: 10.1111/j.1469-7793.1998.415bw.x.

Abstract

1. We have investigated the interactions between intracellular pH (pH1) and the intracellular free calcium concentration ([Ca2+]i) in isolated rat pancreatic acinar cells. The fluorescent dyes fura-2 and BCECF were used to measure [Ca2+]i and pHi, respectively. 2. Sodium acetate and ammonium chloride (NH4Cl) were used to acidify and alkalinize pHi, respectively. Cytosolic acidification had no effect on [Ca2+]i in resting pancreatic acinar cells, whereas cytosolic alkalinization released Ca2+ from intracellular stores. 3. Cytosolic acidification using either acetate or a CO2-HCO3(-)-buffered medium enhanced Ca2+ signals evoked by acetylcholine (ACh) and cholecystokinin (CCK). In contrast, both NH4Cl and trimethylamine (TMA) inhibited Ca2+ signals during stimulation with either ACh or CCK. This inhibitory effect was also observed in the absence of extracellular Ca2+, and was therefore not due to changes in Ca2+ entry. 4. Calcium oscillations evoked by physiological concentrations of CCK were enhanced by cytosolic acidification and inhibited by cytosolic alkalinization. 5. In order to determine the effects of pHi upon Ca2+ handling by intracellular Ca2+ stores, intraorganellar [Ca2+] was monitored using the low affinity Ca2+ indicator mag-fura-2 in permeabilized cells. Addition of NH4Cl, which is expected to alkalinize intraorganellar pH, did not alter intraorganellar [Ca2+] in permeabilized cells, suggesting that changing intraorganellar pH does not release Ca2+ from intracellular stores. Addition of NH4Cl or acetate also did not affect the rate of Ca2+ release induced by inositol 1,4,5-trisphosphate (InsP3). 6. Modification of extraorganellar ('cytosolic') pH did not affect the rate of ATP-dependent Ca2+ uptake into stores, but did modify the rate of Ca2+ release evoked by submaximal concentrations of InsP3. The rate of Ca2+ release was increased at more alkaline extraorganellar pHs. These results would suggest that manipulation of intraorganellar pH does not affect Ca2+ handling by the intracellular stores. In contrast, extraorganellar ('cytosolic') pH does affect InsP3-induced Ca2+ release from the stores. 7. In conclusion, changes in intracellular pH in pancreatic acinar cells can profoundly alter cytosolic [Ca2+]. This may shed light on earlier observations whereby cell-permeant weak acids and bases can modulate fluid secretion in epithelia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetates / pharmacology
  • Acetylcholine / agonists
  • Acetylcholine / pharmacology
  • Ammonium Chloride / pharmacology
  • Animals
  • Calcium / agonists
  • Calcium / antagonists & inhibitors
  • Calcium / metabolism*
  • Cholecystokinin / agonists
  • Cholecystokinin / pharmacology
  • Evoked Potentials / drug effects
  • Evoked Potentials / physiology
  • Hydrogen-Ion Concentration / drug effects
  • Inositol 1,4,5-Trisphosphate / pharmacology
  • Intracellular Fluid / chemistry
  • Organelles / chemistry
  • Organelles / drug effects
  • Organelles / metabolism
  • Pancreas / cytology*
  • Pancreas / drug effects
  • Pancreas / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*

Substances

  • Acetates
  • Ammonium Chloride
  • Inositol 1,4,5-Trisphosphate
  • Cholecystokinin
  • Acetylcholine
  • Calcium