H+ disposal by rabbit gastric mucosal surface cells

Area of Science:

• Cell Physiology
• Gastrointestinal Biology
• Ion Transport Mechanisms

Background:

• Gastric mucosal surface cells face challenges from luminal acid.
• Cellular mechanisms for maintaining intracellular pH are crucial for gastric protection.
• The role of ion exchange in gastric acid defense requires further elucidation.

Purpose of the Study:

• To investigate the role of ion transport in regulating intracellular pH of gastric mucosal cells.
• To determine the involvement of sodium-hydrogen (Na+/H+) exchange in cellular acid defense.
• To explore the influence of extracellular ions, particularly sodium (Na+) and potassium (K+), on this process.

Main Methods:

• Isolated gastric mucosal surface cells were exposed to ammonium chloride (NH4+) to induce intracellular acidification.
• Intracellular pH was measured using the fluorescent dye acridine orange.
• The effects of varying extracellular ion concentrations (Na+, K+) and inhibitors (amiloride, ouabain, valinomycin) on proton gradient dissipation were assessed.

Main Results:

• Ammonium chloride exposure led to intracellular acidification, creating a pH gradient.
• This gradient dissipated in Na+-containing, K+-free solutions, with Na+ addition causing rapid dissipation (half-maximal at 56 mM Na+).
• Sodium-induced gradient dissipation was sensitive to amiloride (half-maximal inhibition at 38 µM) and modulated by K+ concentration.

Conclusions:

• Sodium-hydrogen (Na+/H+) exchange is a key mechanism for gastric mucosal surface cells to protect against diffusing acid.
• This ion exchange process is sensitive to amiloride and is modulated by extracellular potassium concentration.
• The identified Na+/H+ exchange mechanism appears independent of Na+, K+-adenosine triphosphatase activity.