Role of HCO3- ions in cytosolic pH regulation in rat mast cells: evidence for a new Na+-independent, HCO3--dependent alkalinizing mechanism

Biochem Biophys Res Commun. 1998 Dec 18;253(2):320-4. doi: 10.1006/bbrc.1998.9615.

Abstract

The role of external HCO3- in pHi regulation in rat mast cells was studied with BCECF. In a HCO3--free medium cells undergo an alkalinization after the addition of 40 mM HCO3Na. This alkalinization is unaffected by pH. In a Na+-free medium, the addition of 20 mM HCO3Na induced a higher alkalinization than 20 mM HCO3K. Amiloride (1 mM), a Na+/H+ exchanger inhibitor, inhibited by 45% the alkalinization induced by HCO3Na, but it did not change that induced by HCO3K. The anion exchanger inhibitor DIDS reduced 20% the alkalinization induced by both salts. An alkalinization of 0.085 units is observed after the addition of 20 mM HCO3K, even when these exchangers are inhibited (in the absence of Na+ and presence of DIDS). We conclude that the Na+/H+ exchanger and the Cl-/HCO3- exchangers are alkalinizing mechanisms that regulate pHi in these cells. Also, there is some HCO3--dependent, Na+-independent mechanism responsible for the intracellular alkalinization.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alkalies / metabolism*
  • Animals
  • Antiporters / physiology
  • Bicarbonates / metabolism*
  • Bicarbonates / pharmacology
  • Chloride-Bicarbonate Antiporters
  • Chlorides / metabolism
  • Cytosol / metabolism*
  • Hydrogen-Ion Concentration
  • Mast Cells / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Serous Membrane / cytology
  • Sodium / metabolism*
  • Sodium-Hydrogen Exchangers / physiology

Substances

  • Alkalies
  • Antiporters
  • Bicarbonates
  • Chloride-Bicarbonate Antiporters
  • Chlorides
  • Sodium-Hydrogen Exchangers
  • Sodium